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101	[ed. note: These data disagree on the presence of NMDA receptors in the soma. For a full description of the properties of NMDA receptors in CA3 pyramidal neurons, please see the apical dendritic compartments.] Recordings from membrane patches of dendrites and soma reveal fast and slow responses to fast application of glutamate, mediated by AMPA amd NMDA receptors, respectively
102	[ed. note: we are not aware of glutamatergic synapses onto the soma] Recordings from membrane patches of dendrites and soma reveal fast and slow responses to fast application of glutamate, mediated by AMPA amd NMDA receptors, respectively
103	1990) causing hyperpolarization, and presynaptic GABAb receptors causing enhancement of synaptic inhibition (Cameron and Williams, 1993). (Reviewed in
104	2 types: one is a slow I AHP type current; weak in LGN, strong in peritenial; the other is fast.
105	5-HT excites 5-HT2 receptors in interneurons and 5-HT1C receptors in pyramidal neurons
106	5HT increases excitability and input resistance
107	90% of cat brainstem input to LGN is cholinergic
108	A 40-50% reduction in a small fraction of (peri-) somatic synapses with large or complex postsynaptic structure after kindling has been found. This functionally relevant reduction may be related to the loss of a specific class of interneurons, and could underlie the enhanced seizure susceptibility after kindling epileptogenesis
109	A combined in situ hybridization and immunocytochemical study demonstrated that Kv1.2 (which may correspond to I(K) channels) is concentrated in the dendrites of CA3 neurons
110	A combined in situ hybridization and immunocytochemical study demonstrated that Kv1.2 (which probably corresponds to I(K) channels) is concentrated in the dendrites of CA3 neurons
111	A D-type potassium current is involved in dendritic calcium spikes initiation and repolarization
112	A distinction was made between axon-bearing and axon-lacking dendrites.
113	a fast voltage activated potassium current that generates the afterhyperpolarization following a fast spike." (data from
114	A linear increase has been found (9 pA/100um) in the density of these channels with distance from soma. It was suggested that this generates site independence of EPSP time course
115	A long duration component of the spike afterhyperpolarization determined the period of the oscillation and was generated by an apamin-sensitive calcium-activated potassium current..”
116	A non-inactivating, Ca-independent, K+ current may limit the amplitude of membrane depolarizations associated with prolonged excursions into the depolarized state
117	A persistent sodium current was the source of current during the depolarizing phase of the oscillation.”
118	A shift toward more depolarized potentials of the activation curve has also been observed in mid and distal dendrites (more than 100um)
119	A single-electrode voltage-clamp technique was employed on slices to examine slow AHP. This was achieved by using conventional procedures to evoke an AHP in current clamp, followed rapidly by a switch into voltage clamp (hybrid clamp). The AHP current showed a dependence on extracellular K+ close to that predicted by the Nernst equation. It could be blocked by Cd2+ or norepinephrine, showed a requirement for voltage-dependent Ca2+ entry, but did not show any clear intrinsic voltage dependence. Once activated, AHP current is not turned off by hyperpolarizing the membrane potential
120	A slow, noninactivating current may have a role to define the limits on the depolarized state, and to govern the spike discharge characteristics once the depolarized state has been reached
121	A slowly activating, outward rectifying potassium current is present in subpopulation of isolated bipolar cells
122	A slowly inactivating A current has also been studied
123	A study in rat using two-photon microscopy to image calcium transients revealed these channels and suggested a novel mechanism for regulation of lateral inhibition
124	A study indicates that synaptic activation of these receptors increases inhibitory activity in relay neurons by increasing output of presynaptic dendrites
125	A study using simultaneous intracellular recording from interneurons and pyramidal neurons combined with biocytin cell fills and morphological reconstructions revealed that the interneurons made connections onto the soma and proximal dendrites of the pyramidal neuron and that stimulation of the interneurons evoked IPSPs in the pyramidal neurons. EM microscopy revealed differential numbers of terminals depending on the subcellular locus of the connections.
126	A subpopulation of interneurons in layer III of the rat piriform cortex are excited by 5-hydroxytryptamine (5-HT) via 5-HT2A receptors and by norepinephrine via alpha 1-adrenoceptors.
127	A subsequent study in rat slice cultures has shown that bath application of MCPG (a mGluR antagonist) blocks the inward Ca-dependent K-current associated with ACPD application or mossy fiber stimulation in the presence on ionotropic GluR antagonists
128	A-channel regulate timing of dendrodendritic inhibition between Mitral cells and granule cells
129	A-channel regulates timing of dendrodendritic inhibition between mitral and granule cells: The transient IA attenuates dendrodendritic input mediated by fast-acting AMPA receptors, such that the excitation and subsequent inhibitory output of granule cells follows the prolonged kinetics of their NMDA receptors. Altering weights of AMPA and NMDA inputs by modulating IA provides a mechanism to regulate the timing of inhibition. A-channels are localized in dendrites.
130	A-channel regulates timing of dendrodendritic inhibition between mitral and granule cells: The transient IA attenuates dendrodendritic input mediated by fast-acting AMPA receptors, such that the excitation and subsequent inhibitory output of granule cells follows the prolonged kinetics of their NMDA receptors. Altering weights of AMPA and NMDA inputs by modulating IA provides a mechanism to regulate the timing of inhibition. A-channels are localized in dendrites.
131	A-current is reduced in the presence of amyloid-beta
132	acetylcholine receptors.
133	Ach exerted two distinct effects on fast-spiking interneurons: Ach directly depolarized FS interneurons by acting on nondesensitizing soma-dendritic nicotinic receptors. In addition, Ach attenuated the GABAergic inhibition of projection neurons by fast-spiking interneurons through activation of presynaptic muscarinic receptors
134	Achergic neurons are in direct synaptic contact with dopaminergic axons in the rat neostriatum
135	Action potential-evoked Ca2+ signals in spines of basal dendrites decreased slightly with distance from the soma
136	action potential-mediated depolarization can...result in the elevation of dendritic intracellular Ca concentration (Regehr et al 1989,
137	Activation curve was studied using patch clamp recordings
138	Activation of both D1- and D2-class receptors has been shown to modulate potassium and sodium currents in acutely isolated neostriatal neurons
139	Activation of M2-class muscarinic receptors in cholinergic interneurons reduces N- and P-type Ca2+ currents through a membrane-delimited pathway using a Gi/o-class G-protein
140	Activation of mGluR increases GC excitability, an effect that should increase GC-mediated GABAergic inhibition of mitral cells
141	Activation of mGluR1 in Purkinje cells causes a Ca-dependent release of a retrograde messenger, probably Glutamate, which acts on presynaptic ionotropic glutamatergic receptor (AMPA/kinate) on the parallel fibers (PFs), depolarizes PFs and modulates neurotransmission from parellel fibers to Purkinje cells
142	Activation of mGluR5 increases GC excitability, an effect that should increase GC-mediated GABAergic inhibition of mitral cells
143	Activation of muscarinic receptors decreases granule cell firing frequency, as well as modulates GABAergic synaptic inputs onto mitral cells.
144	Activation of the adenosine A1 receptor reduces synaptic strength by modulating presynaptic calcium channels. Baclofen modulates presynaptic calcium channels as well but also affects release processes downstream from calcium entry
145	Activation of the Ca2+ current by depolarization as short as 15 ms in a single bipolar cell evokes the glutamatergic postsynaptic currents, of both both NMDA and non-NMDA types, in the Ganglion cells
146	acts on D2 autoreceptors
147	All Calcium Currents. Low Voltage Activated current increased during development
148	All levels of the apical dendrites receive input from granule cells (which receive their input from mossy fibers); the terminals make small spherical vesicle (ss) synapses
149	also in giant cells, and they interact with each other; SOBiv p135). Cartwheel cells are the second most numerous cell in the DCN, after the granule cells (SOBiv p135).
150	Although both the soma and distal dendrites have both the fast and slow GABAA-mediated IPSCs, there is a greater proportion of slow component in the dendrites. Slow GABAA mediated IPSC component is regulated by presynaptic GABAB inhibition (at the interneuron terminals?) whereas the fast is not
151	AMPA and NMDA receptor mediated cortical glutamatergic inputs that were relatively weak compared to the inputs of SPNs and GABAA receptor mediated inhibitory inputs comparable to those of SPNs.”
152	AMPA and NMDA receptors are clustered, and colocalized, on granule cells dendritic spines.
153	AMPA receptors during development: granule cells express a heterogeneous population of AMPA receptors, a subset of which are segregated to postsynaptic sites after synaptogenesis
154	AMPA receptors postsynaptic to the auditory nerve have relatively fast decay kinetics
155	Amplitudes of excitatory postsynaptic conductances (EPSCs) evoked in RTN neurons by minimal stimulation of corticothalamic fibers were 2.4 times larger than in relay neurons, and quantal size of RTN EPSCs was 2.6 times greater. GluR4-receptor subunits labeled at corticothalamic synapses on RTN neurons outnumbered those on relay cells by 3.7 times
156	Amputation of the apical dendrite approximately 30 micron from the soma, while simultaneously recording the slow AHP whole cell current at the soma, depressed the sAHP amplitude by only approximately 30% compared with control. Somatic cell-attached and nucleated patches did not contain sAHP current. Amputation of the axon about 20um from the soma had little effect on the amplitude of the sAHP. By this process of elimination, it is suggested that sAHP channels may be concentrated in the basal dendrites of CA1 pyramids
157	Analysis of synaptic input to layer 4 basket cells show that 79% of symmetric synapses could have originated from other layer 4 basket cells. Soma and proximal dendrites received 76% of all the symmetric synapses
158	Anatomical, electrophysiological and molecular diversity of basket cell-like interneurons in layers II-IV of rat somatosensory cortex were studied using patch-clamp electrodes filled with biocytin
159	and
160	and by cholinergic agonists in slices
161	and can activate Ca action potentials
162	and inside-out membrane patches
163	and it has been shown that nimodipine (an L-channel antagonist) prevents certain mossy fiber LTP-types from taking place
164	and nicotinergic
165	and Shepherd GM ed. Synaptic Organization of the Brain, 1998. p182) GABA release onto mitral: spontaneous and gltamate-evoked. Moreover, activation of muscarinic receptors modulates GABAergic synaptic inputs onto mitral cell.
166	and Shepherd GM ed. Synaptic Organization of the Brain, 1998. p182)GABA release onto mitral: spontaneous and gltamate-evoked. Moreover, activation of muscarinic receptors modulates GABAergic synaptic inputs onto mitral cell.
167	and stain for postsynaptic GLYR
168	Another study suggested that adult neostriatal projection neurons do not express significant levels of LVA Ca2+ current
169	Another study using bath application of 1S,3R-ACPD in rat slice cultures during single electrode voltage clamp recording showed that depolarizing current steps revealed a suppression of K currents leading to a negative slope conductance at potential between -55mV and -40 mV
170	AP propagation was studied in the somas and dendrites of intact retinal ganglion cells exposed by enzymatic removal of the overlying endfeet of the Muller glia. Simultaneous somatic and dendritic whole cell patch recordings suggested that the dendrites of retinal ganglion cells support Na+ AP.
171	Apical dendrites of L6 pyramidal neurons in somatosensory cortex are similar to L5 and L2/3 in that they includeNMDA-dependent electrogenesis
172	Application of acetylcholine (ACh) evoked concentration-dependent whole-cell currents
173	Assumed.
174	At least 40% of choline acetyltransferase-immunopositive cholinergic interneurons were immunopositive for GluR1 or GluR4
175	At parallel fiber (PF) -Purkinje cell synapses, NMDA reversibly depresses postsynaptic currents, through a trans-synaptic mechanism that involves release from PFs nitric oxide that decreases the glutamate sensitivity of the Purkinje cell
176	At the subcellular level in the substantia nigra pars reticulata (SNr), GlyRs show a localized distribution on the soma and dendrites that partially complements but does not overlap with the distribution of gamma-aminobutyric acid (GABA)A receptors."
177	Autaptic self-innervation of basket cells
178	Auto-activation from glutamate released by mitral cell secondary dendrites
179	Auto-activation from glutamate released by mitral cell soma
180	Baclofen suppresses field potentials at the intrinsic fiber synapses proximal to the pyramidal cell bodies (layer Ib) but not field potential at distal dendrites (layer Ia). afferent and intrinsic synaptic inputs may be differentially modulated by the activation of GABAB receptors and that this selective suppression is at least partially mediated via a presynaptic mechanism (at the interneuron terminals?)
181	Basal dendrites receive flattened (FL) and pleiomorphic (PL) synapses (90% of total synapses on proximal dendrites, 62% on distal dendrites) (SOBiv p131). Vertical cells stain for glycine
182	Basket cell activation elicits IPSPs in Purkinje cells
183	Basket cells make synaptic contact with pyramidal and spiny stellate cells preferentially on the somata (50%) and dendritic shaft (45%), but synapses on dendritic spines are also present (4.9%). IPSPs elicited in the postsynaptic cells have short latency, fast rising time and short duration, similar to those mediated by GABAA receptors
184	Bath application of omega-conotoxin MVIIC (an antagonist of N and P channels) blocked (with slow kinetics) approximately 30% of the high-voltage activated Ca2+ current measured in whole-cell recordings
185	Bath application of omega-conotoxin MVIIC blocked (with rapid kinetics) approximately 20% of the high-voltage activated Ca2+ current, suggesting the presence of N-channels measured in whole-cell recordings
186	Bath application of Pb2+ shifted the neurons curent-voltage relation in patch-clamp recording from acutely isolated pyramidal neurons. These results were interpreted to "demonstrate that Pb2+ in micromolar concentration is a voltage-dependent, reversible blocker of delayed-rectifier potassium currents of hippocampal neurons"
187	Bath application of Pb2+ shifted the neurons'' current-voltage relation in patch-clamp recording from acutely isolated pyramidal neurons. These results were interpreted to "demonstrate that Pb2+ in micromolar concentration is a voltage-dependent, reversible blocker of delayed-rectifier potassium currents of hippocampal neurons"
188	Benardo et al 1982;
189	Bicuculline disrupts timing of odor_evoked responses
190	Blockade of fast spike by TTX
191	blocked by strychnine. Ia IPSPs are located near the cell soma
192	Both HVA and LVA calcium currents were present in cell bodies of identified neurons. P/Q-type channels accounted for only 6 % of HVA, while L-, N- and R-type Ca2+ channels each accounted for around one-third of the somatic calcium current.
193	Both ionotropic NMDA and non-NMDA autoreceptors are activated by glutamate released from primary and secondary dendrites. In contrast to non-NMDA autoreceptors, NMDA autoreceptors are almost exclusively located on secondary dendrites and their activation generates a large and sustained self-excitation. Both intracellularly evoked and miniature NMDA-R mediated synaptic potentials are blocked by intracellular BAPTA and result from a calcium-dependent release of glutamate
194	Both X and Y relay neurons receive inputs from TRN axons. The X neurons are innervated both within the glomerulus and above the glomerulus on the middle of the denritic tree (SOBIV p301, 305).
195	but not LTP or LTD (SOBiv p90).
196	but not LTP or LTD (SOBiv p90).Motoneurons have a high density of AMPA receptors (Vandenberghe et al, JNS 20: 7158, 2000). There is evidence that "glutamate receptor-mediated Ca2+ influx, intracellular Ca2+ accumulation, and subsequent cell death" may be involved in the mechanism of selective motoneuron degeneration in amyotrophic lateral sclerosis.
197	but not LTP or LTD (SOBiv p90).Postnatal development and properties of these receptors were studied with whole-cell and outside-out patch-clamp. The conductance and relative distribution were independent of age from postnatal day 4 to 14. The results also suggested that their properties differ from those in spinal cord interneurons
198	but the postsynaptic target is most likely amacrine cells (SOBiv p238).
199	By combining intracellular recordings and two-photon microscopy imaging of [Ca]i in rat it was shown that APs backpropagate at full amplitude up to the tuft
200	By combining intracellular recordings and two-photon microscopy imaging of [Ca]i it was shown that AP propagate at full amplitude up to the most distal branches
201	by contrast,
202	By using dendritic recordings and calcium transients in rats it was shown that this current may control AP propagation in lateral dendrites
203	Ca -dependent Chloride current at the presynaptic terminals of goldfish retinal bipolar cells
204	Ca fluorescence imaging shows that application of L-channel antagonists reduces the Ca influx associated with backpropagating action potentials, and has a significantly greater effect in the proximal dendrites than in more distal dendrites
205	Ca fluorescence imaging shows that application of N-channel antagonists slightly reduces the Ca influx associated with backpropagating action potentials
206	Ca fluorescence imaging shows that application of P-channel antagonists reduces the Ca influx associated with backpropagating action potentials
207	Ca-dependent potassium currents are seen in dissociated cells
208	CA1 neurons and subiculum neurons in hippoampus differ in firing pattern (the former being regular and the later being either regular, weakly bursting or strongly bursting) and resting membrane properties (such as input restistance and membran time constant); however, low concentration of 4-AP (50 &#181M) can convert neurons in both regions into firing bursting action potentials
209	CA1 neurons and subiculum neurons in hippoampus differ in firing pattern (the former being regular and the later being either regular, weakly bursting or strongly bursting) and resting membrane properties (such as input restistance and membran time constant); however, low concentration of 4-AP (50 ?M) can convert neurons in both regions into firing bursting action potentials
210	CA1 neurons and subiculum neurons in hippoampus differ in firing pattern (the former being regular and the later being either regular, weakly bursting or strongly bursting) and resting membrane properties (such as input restistance and membran time constant); however, low concentration of 4-AP (50 µM) can convert neurons in both regions into firing bursting action potentials
211	CA1 pyramidal neurons increase their firing (recorded extracellularly) in response to ionophoresed Glu within their apical dendritic fields or in the cell body layer (Dudar 1974 PMID#4437726).
212	Ca2+ -activated K+ current at presynaptic terminals of goldfish retinal bipolar cells
213	Ca2+-activated K+ currents were studied using whole-cell patch-clamp recordings from freshly dissociated mouse neocortical pyramidal neurons
214	Calcium entry through N-type calcium channels (CaV2.2) causes activation of KCa channels that decrease the firing rate and increase the regularity of firing in SNr GABA neurons”
215	Calcium influx through NMDA receptors can directly trigger presynatic GABA release for local dendrodendritic feedback inhibition. DDI is elicited by photorelease of caged Ca++, with and without Cd++ and Ni++.
216	Calcium influx through NMDA receptors directly evokes GABA release in granule cells.
217	Calcium is involved in delayed release of neurotransmitter at synapses between granule cell their postsynaptic targets (stellate cells and Purkinje cells)
218	Calcium-dependent potassium channels are preferentially activated by calcium entry through N- and Q-type channels
219	CaV channels are among the intrinsic membrane channels influencing the excitability of the SNr neuronal membrane. CaV channels have been shown to influence spontaneous activity in these neurons, as well as more complex behaviors such as plateau potential generation burst firing.”
220	Cell-attached dendritic recordings in rats up to about 60um from the soma showed that low-threshold calcium channels were concentrated at proximal dendritic locations, sites known to receive excitatory synaptic connections from primary afferents, suggesting that they play a key role in the amplification of sensory inputs to TC neurons
221	Cell-attached patches on the proximal 100um of the apical dendrite did not contain sAHP channels. Amputation of the apical dendrite approximately 30 micron from the soma, while simultaneously recording the sAHP whole cell current at the soma, depressed the sAHP amplitude by only approximately 30% compared with control. Somatic cell-attached and nucleated patches did not contain sAHP current. Amputation of the axon about 20um from the soma had little effect on the amplitude of the sAHP. By this process of elimination, it is suggested that sAHP channels may be concentrated in the basal dendrites of CA1 pyramids
222	Cell-attached recordings in rats up to about 60um from the soma demonstrated a non-uniform dendritic distribution of channels
223	Cell-attached recordings in rats up to about 60um from the soma demonstrated a roughly uniform density of channels across the somatodendritic area examined that corresponds to approximately half the average path length of TC neuron dendrites
224	Cell-specifc modulation of GABAA receptor- mediated chloride current by dopamine. In interneurons (mainly granule cells), dopamine reduces GABAA Cl- current, via D1 receptor and involves phosphorylation of GABAA receptors by PKA. In mitral cell, dopamine enhances GABA responses via activation of D2 receptors and phosphorylation of GABAA receptors via PKC.
225	Cell-specifc modulation of GABAA receptor- mediated chloride current by dopamine. In interneurons (mainly granule cells), dopamine reduces GABAA Cl- current, via D1 receptor and involves phosphorylation of GABAA receptors by PKA. In mitral cell, dopamine enhances GABA responses via activation of D2 receptors and phosphorylation of GABAA receptors via PKC.
226	Cells acutely dissociated from slices obtained from chronic temporal lobe epilepsy patients displayed a high-voltage activated Ca2+ conductance with a pronounced Ca2+-dependent inactivation
227	Cells were voltage-clamped using a single microelectrode, at 23-30 degrees C. M-current resembled that of sympathetic ganglion cells. It was abolished by addition of carbachol, muscarine or bethanechol, as well as by 1 mM barium. It was suggested that activation of cholinergic septal inputs to the hippocampus facilitates repetitive firing of pyramidal cells by turning off the M-conductance, without much change in the resting potential of the cell
228	Cerebellar granule cells from young rats (postnatal days 1-9) possess voltage-activated inward Na+ current as well as two types of K+ current, IA and IK
229	Chen et al 1997). Dendritic patch recordings showed an even density of Na channels (120pS um-2) up to 350 um from the soma along the primary dendrite to the origin of the glomerular tuft
230	Chen et al 1997).Dendritic patch recordings showed an even density of Na channels (120pSum-2) up to 350 um from the soma along the primary dendrite to theorigin of the glomerular tuft
231	Choline acetyltransferase immunocytochemistry shows that cholinergic projections from the basal forebrain to the main olfactory bulb focus synaptic innervation on interneurons, on the dendritic spines of periglomerular and granule cells.
232	Cholinergic agonist carbachol caused a significant suppression of inhibitory postsynaptic potentials (IPSPs) in the pyramidal neurons that were induced by stimulation of layer Ib, with a weaker effect on IPSPs induced by stimulation of layer Ia
233	Cholinergic agonist carbachol selectively suppresses intrinsic fiber synaptic potentials but not afferent fiber synaptic potentials.
234	Cholinergic agonist carbachol selectively suppresses intrinsic fiber synaptic potentials but not afferent fiber synaptic potentials. A presynaptic mechanism of cholinergic suppression is suggested
235	Cholinergic agonist carbachol selectively suppresses intrinsic fiber synaptic potentials but not afferent fiber synaptic potentials. (Hasselmo ME and Bower JM, 1992353 ) (Patil MM and Hasselmo ME, 1999341 ).
236	Cholinergic interneurones in rat exhibit a ATP-sensitive potassium channel current. sigle-cell-RT-PCR shows that this channel is formed from Kir6.1 and SUR1 subunits
237	cited in Johnston and Amaral, 1998).
238	Clusters of glycine receptors were found on the somatodendritic membranes of Alpha ganglion cells
239	Clusters of the alpha1, and alpha2, alpha3, and gamma2 subunits of the GABAA receptor were found on the somatodendritic membranes of Alpha ganglion cells. Experiments with different combinations of the subunit-specific antibodies showed that the alpha1, alpha2, and alpha3 subunits of the GABA(A) receptor are not colocalized within the same clusters, suggesting that an individual neuron can express several isoforms of the GABAA receptor and that these different isoforms are aggregated at distinct postsynaptic sites
240	Combining preembedding and postembedding immunostaining at the EM level, GluR2/3 and NMDAR1 immunoreactivity was located in somata and in proximal and distal dendrites
241	Conduction of the action potential suggests there must be some Na channels there.
242	Cultured cells
243	Cultured cells; blocked by 100 uM Cd or nifedipine (IC50=368 nM); no T-type Ca channels found
244	Cultured cells; TTX-sensitive
245	Curare blocks responses to applied ACh.
246	D2 dopamine receptors reduce N-type Ca2+ currents in rat neostriatal cholinergic interneurons
247	D5 and D2 dopamine receptors induce "depolarization and an increase in input resistance in striatal FSI in brain slices"
248	DA is released from dendrites
249	DA receptors in mitral cell dendrites implied by DA localization in PG dendrites presynaptic to mitral dendrites
250	DDI (dendrodendritic inhibition) can be elicited by activation of AMPA receptors, while NMDA receptor activation is not an absolute requirement. DDI is blocked by Cd and toxins to N- and P/Q-type channels.
251	DDI (dendrodendritic inhibition) can be elicited by activation of AMPA receptors, while NMDA receptor activation is not an absolute requirement. DDI is blocked by Cd and toxins to N- and P/Q-type channels.
252	Deep multipolar cells have GABA-containing terminals arranged in baskets around pyramidal cell bodies
253	Delayed firing of action potentials in response to current pulse injection suggests there is I A current here. Unpublished data have characterized the kinetics of A current in the rat mitral cell
254	Delayed rectifier. (See SOBiv p140).
255	Dendritic can fire sodium spikes that can precede somatic action potentials (APs), the probability and amplitude of which depend on previous synaptic and firing history. Some dendritic spikes could occur in the absense of somatic APs, indicating that their propagation to soma is unreliable
256	Dendritic fluorescence imaging showed that Ca2+ channels of several subtypes mediated the AP-evoked fluorescence transient in the proximal (100-170 microns) apical dendrite. The fluorescence resulted from Ca2+ entry through L, N, and P-type channels, and through Ca2+ channels (R-type) not sensitive to L-, N- and P-type Ca2+ channel blockers
257	Dendritic GABAA-mediated IPSPs act largely independent of somatic IPSPs and may regulate facilitation of MNDA-mediated respnses
258	Dendritic patch recordings showed an even density of Na channels (120pS um-2) up to 350 um from the soma along the primary dendrite to the origin of the glomerular tuft
259	Dendritic patch recordings showed an even density of Na channels (120pSum-2) up to 350 um from the soma along the primary dendrite to theorigin of the glomerular tuft
260	Dendrodendritic from granule cell spines. IPSP blocked by bicuculline and low Cl-
261	Dendrodendritic inhibition (DDI) between mitral and granule cells relies on N-and P/Q- type calcium channels. Magnitude of DDI is proportional to dendritic calcium influx.
262	Dendrodendritic inhibition (DDI) between mitral and granule cells relies on N-and P/Q- type calcium channels. Magnitude of DDI is proportional to dendritic calcium influx.
263	Dendrodendritic inhibition between mitral and granule cells involves N-and P/Q- type calcium channels. The magnitude of DDI is proportional to dendritic calcium influx.
264	Dendrodendritic inhibition between mitral and granule cells involves N-and P/Q- type calcium channels. The magnitude of DDI is proportional to dendritic calcium influx.
265	Dendrodendritic synapse onto mitral/tufted cells, of type 2
266	Densities and kinetics were measured from patch clamp recordings
267	Depolarisations beyond -40 mV activated a fast transient TTX-sensitive inward current. Once activated, INa declined exponentially to zero following a single exponential. The underlying conductance showed a sigmoidal activation between -40 and +30 mV, with half activation at -17.4 mV and a maximal value of 9.7 nS per neurone. The steady-state inactivation was complete at -30 mV and completely removed at -90 mV, with a midpoint at -56 mV. The activation process could be adequately described by third order kinetics, with time constants ranging from 260 microseconds at -20 mV to 70 microseconds at +50 mV.
268	Depolarization induced transient outward currents that resembled IPSCs and were blocked by GABA and glycine receptor antagonists, suggesting that they arise from activation of amacrine feedback synapses
269	Depolarizes SNr principle cells. Generated by subset of voltage-gated sodium channels that remain open for extended periods of time. Can contribute to neuronal excitability and pacemaking activities.
270	Depolarizing "sag" during larger hyperpolarizing voltage transients is indicative of Ih current in determinating the passive membrane properties of CA1 pyramidal neurons
271	Different GABAergic receptors are localized to specific layers, and may mediate feedforward and feedback inhibitions
272	Differential GABABergic presynaptic modulation in layers Ia and Ib: While baclofen suppresses field potentials at the intrinsic fiber synapses proximal to the pyramidal cell bodies (layer Ib), it does not affect field potentials at distal dendrites (layer Ia)
273	Differential induction of potentiation and depression at commissural and mossy fiber synapses has also been shown by
274	Differential induction of potentiation and depression at commissural and mossy fiber synapses has also been shown by #R#158#E#. Recordings from membrane patches of dendrites and soma reveal fast and slow responses to fast application of glutamate, mediated by AMPA amd NMDA receptors, respectively
275	discussed in Burke 1998).
276	Dopamine modulates Ih in cultured rat olfactory receptor neurons
277	Dopaminergic afferents from substantia nigra pars compacta” target the globus pallidus.
278	Dopaminergic subdivision of the periglomerular interneurons throughout classes of vertebrates.
279	Dual patch recordings and Ca2+ imaging of mitral cells in the rat olfactory bulb slice suggested that action potentials propagating into the basal dendrites decrement approximately 20% per 100um
280	Dual patch recordings and Ca2+ imaging of mitral cells in the ratolfactory bulb slice suggested that action potentials propagating intothe basal dendrites decrement approximately 20% per 100um
281	Dual patch-clamp recordings showed that Ca-activated K+ (BK) channels were not triggered by neuronal action potentials in normal slices and only opened as neuronal responses deteriorated (smaller or absent spikes) and in a spike-independent manner, suggesting that BK channels may activate only in pathological conditions
282	Dual recording from pyramidal cell-basket cell pairs reveal unitary EPSPs in basket cells mediated by one and two synaptic junctions. The unitary EPSPs have fast rising time and short time duration. Closely timed (10-50 ms) pairs of presynaptic action potentials resulted in statistically significant paired-pulse depression. The reliability of transmission is high, but the fast time course of the EPSPs constrains their temporal summation. Due to the relatively small amplitude of unitary EPSPs several convergent inputs will therefore be required to elicit suprathreshold responses.
283	Dual whole-cell recordings in acute slices showed that kainate receptors located on presynaptic interneuron terminals can be activated by glutamate released from the somatodendritic compartment of the postsynaptic pyramidal cells
284	Dual whole-cell recordings in connected cell pairs suggested that attenuation of local horizontal excitation by dopamine is through D1 actions at a presynaptic site
285	Dual whole-cell recordings showed that Ca2+-dependent release of a retrograde messenger, most probably glutamate, from dendrites suppresses the inhibition of pyramidal neurons
286	During periods of induced regular firing, intrastriatal stimuli were used to evoke pharmacologically isolated monosynaptic AMPA receptor-mediated EPSPs or GABAA receptor-mediated IPSPs. EPSPs evoked during the interspike interval (ISI) produced a phase-dependent decrease in the ISI, whereas IPSPs produced a phase-independent prolongation of the ISI
287	Each isoform [of Na channel] was found within neuronal somata and dendrites of all diameters within the GP".
288	Effects of odorants on this current in newt ORNs were investigated using whole-cell patch-clamp
289	Electrophysiological classification of juxtaglomerular neurons: bursting and standard firing. In contrast to the standard firing neurons, bursting neurons produced a calcium-channel-dependent low-threshold spike (LTS) when depolarized either by current injection or by spontaneous or evoked postsynaptic potentials. Bursting neurons also could oscillate spontaneously. Most bursting cells were either periglomerular cells or external tufted cells. Based on their mode of firing and placement in the bulb circuit, these bursting cells are well situated to drive synchronous oscillations in the olfactory bulb. LVA (low voltage-activated) Ca++ channel may be involved in LTS.
290	Electrophysiological evidence shows that N-channels and L-channels are present in all dendritic compartments in turtle motoneurons
291	Electrophysiology data: AP5 attenuates delayed excitatory components in peristimulus time histograms of mitral cell unit responses to olfactory nerve volleys
292	Electrophysiology data: DNQX attenuates early and late excitatory components in peristimulus time histograms of mitral cell unit responses to olfactory nerve volleys
293	EM evidence for GABAergic input to deeper dendritic layers
294	EM showed colocalization at axodendritic asymmetric synapses within the CA1 subfield of rat hippocampus. AMPA/NMDA receptor colocalization was found in non-GABAergic dendritic shafts as well as dendritic spines, suggesting that excitatory neuronal transmission in CA1 neurons may generally involve activation of both NMDA and AMPA receptor subunits at a single synapse
295	Estimated: HH model slightly modified from
296	Estimated: HH model slightly modified from Traub, 1982
297	Evidence from intracellular responses to nicotine, but not to oxotremorine
298	Evidence of presence of high-threshold calcium channel
299	Evidence of spatial and temporal facilitation of fast IPSPs, interpretated as the convergence of excitatory input onto the inhititory interneurons from different olfactory structures
300	Experimental findings support a cascade for induction of homosynaptic, NO-dependent LTD involving activation of guanylyl cyclase, production of guanosine 3',5' cyclic monophosphate and subsequent PKG activation. This process has an additional requirement for release of Ca2+ from ryanodine-sensitive stores
301	Extracelluar ACPD (an mGluR agonist) application to apical or basal dendrites of CA1 pyramidal neurons causes local increases in calcium concentration that propagate throughout the cell, as measured by simultaneous whole cell recording and confocal microscopy with calcium imaging
302	Extracellular recordings in vivo suggested that the dendritic density of these channels rapidly decreases with distance from soma
303	Fast IPSP, blocked by bicuculline and low Cl-
304	for review see Llinas and Walton 1998).
305	found an NMDA component in neonatal rat. Short-term post-tetanic potentiation (PTP) and depression (PTD) occur
306	found evidence for the presence of GABAB receptors on cell dendrites. Recordings in slices showed that GABA inhibition was mediated by GABA(B) receptors in the dendrites and GABA(A) receptors in the soma and dendrites. Therefore, the GABA released by stellate cells modulates Purkinje cells activity through two inhibitory mechanisms
307	From cerebral cortex
308	From rodents to primates, the SNr and GPi innervate thalamic and brain stem nuclei connected to motor, prefrontal, parietal and temporal associative cortical areas offering an access for BG to control motor, cognitive, as well as emotional–motivational processes.”
309	FSIs “have GABAergic inputs originating from the GP. The pallidostriatal inputs are largely selective for FSIs (Bevan et al., 1998) and in vivo, increased firing of FSI during choice selection in a simple discrimination task coincide with a decrease in firing of GP neurons .”
310	GABA and glycine conductances of isolated bipolar cells
311	Gaba being from Amacrine Cells
312	GABA from basket cell inhibitory interneurons.
313	GABA from chandelier inhibitory interneurons.
314	GABA from some Renshaw interneurons; IPSPs are Cl- mediated, potentially blocked by picrotoxin
315	GABA inactivation of large-basket cells of visual cortex resulted in weakened orientation and direction selectivity, via weakening of long-range lateral inhibition by the basket cells
316	GABA is a neurotransmitter used by basket cells or clutch cells
317	GABA is the transmitter released from large superficial horizontal cells and small globular-soma cells which mediate feed-forward inhibition of the pyramidal neurons when activated by axon terminals of mitral/tufted cells in the lateral olfactory tract or association fibers from other pyramidal neurons
318	GABA(A) and GABA(C) receptor-mediated currents were observed in the isolated terminal
319	GABA(A) receptors mediate GABAergic inhibition on bipolar cell dendrites in the OPL, that GABA(A) and GABA(C) receptors mediate inhibition on axon terminals in the IPL, and that the GABA(C):GABA(A) on the terminals may tune the response characteristics of the bipolar cell
320	GABA(A)-mediated (bicuculline-sensitive) inhibitory responses can be demonstrated in CA1 neurons by extracellular recording (Curtis et al, 1970) and by recording spontaneous synaptic currents (Collingridge, 1984).
321	GABAB receptors act presinaptically to regulate the release of glutamate from olfactory nerve terminal
322	GABAergic inhibitory synapses onto mitral cells, through dendrodendritic spine synapse: possibly two types: self inhibition and lateral inhibition.
323	GABAergic interneurons (basket cells, dendrite-targeting cells, and double-bouquet cells) form reciprocally interconnected intracortical networks in which basket cells play a prominent role, given the strength of innervation and the proximal placement of synapses by basket cells to their postsynaptic targets
324	GABAergic interneurons in deeper layers of piriform cortex receive symmetric synapses as well as asymmetric synapses
325	GABAergic responses evoked by electrical stimulations have been studied in slices
326	GABAergic synaptic inputs originating from the globus pallidus were also demonstrated ultrastructurally using juxtacellular labeling and NOS immunocytochemistry.”
327	GAD-positive gemmules (spines) of granule cells were observed to form reciprocal dendrodentritic synaptic junctions with mitral cell dentrites which lacked reaction product.
328	GAD-positive staining
329	GAD-positive staining gemmules (i.e., spines) of periglomerular cells also formed reciprocal dendrodentritic synaptic contacts with mitral/tufted cell dentrites.
330	GLU acts on both AMPA and NMDA receptors
331	Glu from Ia axon terminals (reviewed in
332	GLU is the primary excitatory transmitter of association fiber terminals
333	GLU is the primary excitatory transmitter of the afferent fiber terminal of mitral and tufted cells
334	Glutamate - kainate receptor (glur6)In mouse hippocampal slices, bath application of kainate caused presynaptic reduction in epscs at mossy fiber synapses on CA3 pyramidal cells in glur6 knockouts but not in glur5 knockouts.
335	Glutamate is commonly believed to be the primary excitatory neurotransmitter in the hippocampal formation generally (reviewed in Cotman et al., 1995), and in CA1 in particular
336	Glutamate is released from Ia terminals
337	Glutamate release from parallel fibers (of granule cells) activates AMPA, mGluR on Purkinje cells
338	Glutamatergic fibers originated in the subthalamic nucleus and, to a lesser extent, in the cerebral cortex and thalamus” target the globus pallidus.
339	GLY ionophoresis mimics Ia IPSPs (reviewed by
340	Glycine and GABA elicit concentration-dependent desensitizing currents mediated by chloride.
341	Glycine and GABA exert inhibitory actions on olfactory bulb neurons, mitral/tufted cells, granule and periglomerular cells).
342	Glycine from some Renshaw interneurons; IPSPs are Cl- mediated, potentially blocked by strychnine
343	granule cell dendrodendritic synapses:
344	granule cells are GABAergic:
345	Granule cells compensate for the lack GABAA receptors (in somatic location? ) by expressing the two-pore-domain K+ channel TASK-1, a voltage-independent K + conductance so as to maintain normal neuronal behaviour; this finding highlight the importance of GABAA receptor-mediated background inhibition
346	Granule cells that lack GABAA receptors (in somatic location? ) express the two-pore-domain K+ channel TASK-1, a voltage-independent K + conductance, so as to maintain normal neuronal behaviour
347	Group III mGluRs mediate a direct suppression of bipolar cell transmitter release, through a mechanism of presynaptic autoreceptors
348	Half of the cells from the study
349	have glycine receptors.
350	have provided evidence for active properties. Dual patch recordings show backpropagating impulses
351	High concentration of NE acts at Alpha1 receptors to increase GC excitability and increase GABAergic inhibition inhibition of MC
352	High concentration of NE acts at Alpha2 receptors to decrease GC excitability and decrease GABAergic inhibition inhibition of MC
353	High-voltage-activated (HVA) and low-voltage-activated (LVA) Ca2+ currents were observed in the isolated rod bipolar cell terminal recordings
354	Hilar stimulation has been used to elicit (pharmacologically isolated) IPSPs in CA3 pyramidal neurons (recorded by means of intracellular or whole cell methods depending on the age of the animal). Paired pulse stimulation in this preparation resulted in paired pulse depression, which could be reduced by bath application of CGP35348 (a GABA(B)R antagonist) in adult rats. Neonatal rats (5-7 days old) showed paired pulse depression only within a much shorter range of interstimulus intervals and it was not affected by CGP35348 unless transmitter release was facilitated by raising the bath [Ca2+] and lowering the bath [Mg+]
355	Histochemical studies have established that SNr receivesdense 5-HT innervation originating from 5-HT neurons inraphe nuclei.”
356	histological experiments found Ih expressed in many olfactory bulb cell types including periglomerular cells.
357	histology experiments found Ih in granule cells.
358	Horizontal cells in layer Ia are labelled for GAD and GABA, but not for GABA takeup, suggesting lack of local axon collaterals or high-affinity GABA takeup sites
359	However, channel density varied widely in the proximal compartment, possibly indicating the presence of hot spots.
360	However, in a few apical patches the channel density was increased X 3, which could indicate channel clustering. Ca fluorescence imaging shows that application of T-channel antagonists reduces the Ca influx associated with backpropagating action potentials, and has a two-fold greater effect in the dendrites than in the soma
361	However, in a few apical patches the channel density was increased X 3, which could indicate channel clustering. Ca fluorescence imaging shows that application of T-channel antagonists reduces the Ca influx associated with backpropagating action potentials, and has a two-fold greater effect in the dendrites than in the soma
362	However, in a few apical patches the channel density was increased X 3, which could indicate channel clustering. Ca fluorescence imaging shows that application of T-channel antagonists reduces the Ca influx associated with backpropagating action potentials, and has a two-fold greater effect in the soma than in the dendrites
363	However, in guinea pigs, a combination of high-speed imaging and simultaneous intracellular recordings showed that direct depolarization of the soma or dendrites never caused dendritic [Na+]i increases, suggesting that the climbing fiber-activated [Na+]i changes in the dendrites are due to Na+ entry through ligand-gated channels
364	However, recordings in slices showed that D1 receptor activation can either inhibit or enhance evoked activity, depending on the level of membrane depolarization, by modulating an L-type Ca2+ conductance
365	I M may contribute to a sag and rebound of voltage response to hyperpolarizing current steps
366	Ia EPSPs are mediated largely by AMPA receptors (muscle afferents:
367	Ia IPSPs are chloride mediated
368	Ia IPSPs are readily affected by soma current or Cl- injection, indicating location at the soma or proximal dendrites
369	Ia synapses are immunoreactive for GLU
370	Identification of subunit mRNAs
371	Ih conductance causes voltage attunuation and is more concentrated in dendrites than in soma
372	Ih current: slowly developing hyperpolarisation-activated current with a threshold generally positive to resting potential and with a strongly voltage-dependent activation time constant. The current was Na+- and K+-sensitive, suppressed by external Cs+, and insensitive to Ba++. The Ih should be tonically active at rest, and may contribute to the oscillatory behaviour of the bulbar network
373	Immunochemical evidence of glutamate as neurotransmitter in the terminals of parallel fibers
374	Immunocytochemistry and in situ hybridisation showed that NMDAR1 was expressed in most CN neuronal types, including the fusiform cell apical dendrites. However, fusiform cell basal dendrites, which are the synaptic sites of cochlear nerve fibers, did not express NMDAR1
375	Immunohistochemical evidence shows that CaV1.3 (an L type channel; seeMembrane Properties Resource) is present in soma and all dendritic compartments in turtle motoneurons
376	Immunohistochemical evidence shows that CaV1.3 is present in soma and all dendritic compartments in turtle motoneurons
377	Immunolabeling was observed in soma and dendrites of layer V pyramidal cells in the frontal cortex
378	Implied by current clamp recording of action potential at soma
379	Implied by data on more proximal dendritic regions; still to be tested
380	Implied by Glu released by other compartments of the mitral cell (Dale's law). Target (destination) is presumably PG cell dendrites in the glomerulus
381	Implied by recording of fast prepotential. Dual patch recordings provide evidence for both backpropagating and forward-propagating impulses in the primary dendrite
382	Implied from evidence that local interneurons colocalize FMRFamide and GABA
383	Importance for membrane excitability of an GABAB receptor-activated inward-rectifying potassium current, sensitive to pertussis toxin and barium
384	In a study of acutely isolated rat cells under whole cell recording across development states (Day 6 - Day 29), it was found that delayed rectifier currents decayed along a double-exponential time course and were 50% blocked by TEA (tetraethylammonium, a I(K) antagonist) at +30 mV at a concentration of about 1mM, as well as being partially blocked by 4-AP (4-aminopyridine). The current also appeared to increase over this development period. This increase was approximately 300% much larger in CA1 cells than in CA3 cells, with only approximately 50%
385	In a study of acutely isolated rat cells under whole cell recording across development states (Day 6 - Day 29), it was found that delayed rectifier currents decayed along a double-exponential time course and were 50% blocked by TEA (tetraethylammonium, a K(DR) antagonist) at +30 mV at a concentration of about 1mM, as well as being partially blocked by 4-AP (4-aminopyridine). The current also appeared to increase over this development period. This increase was approximately 300% much larger in CA1 cells than in CA3 cells, with only approximately 50%
386	In a study of acutely isolated rat cells under whole cell recording across development states (Day 6 - Day 29), it was found that delayed rectifier currents decayed along a double-exponential time course and were 50% blocked by TEA (tetraethylammonium, a K(DR) antagonist) at +30 mV at a concentration of about 1mM, as well as being partially blocked by 4-AP (4-aminopyridine). The current also appeared to increase over this development period. This increase was approximately 300% much larger in CA1 cells than in CA3 cells, with only approximately 50%
387	In a study of acutely isolated rat cells under whole cell recording across developmental states (Day 6 - Day 29), I(A) was separated from I(K) by subtraction methods. It was found that I(A) was rapidly activated and inactivated and was 80% blocked by 4-AP (4-aminopyridine), but was insensitive to TEA (tetraethylammonium) and dendrotoxin (Klee et al, 1995). The current has also been shown to be modulated by K concentration (Eder et al, 1996), though this effect appears to be restricted to very early in development (Klee et al, 1997).
388	In addition, IP3 gated ion channel; found in the autodendritic membrane
389	In an immunocytochemical study in zebrafish 60-70% of cells showed KA receptor mediated labelling
390	In an immunocytochemical study in zebrafish 60-70% of cells showed KA receptor mediated labelling
391	In an immunocytochemical study in zebrafish all cells resulted in NMDA receptor mediated labelling
392	In cell-attached patch-clamp recordings from the soma in guinea pig hippocampal slices, L-currents were found in 34% of the patches and found to have single channel conductances of 23-27 pS
393	In cell-attached patch-clamp recordings from the soma in guinea pig hippocampal slices, L-currents were found in 34% of the patches and found to have single channel conductances of 23-27 pS (Johnston et al. 1992;
394	In cell-attached patch-clamp recordings from the soma in guinea pig hippocampal slices, N-currents were found in 63% of the patches and found to have single channel conductances of 14 pS (Johnston et al. 1992;
395	In cell-attached patch-clamp recordings from the soma in guinea pig hippocampal slices, T-currents were found in 72% of the patches and found to have single channel conductances of 8 pS
396	In cell-attached patch-clamp recordings from the soma in guinea pig hippocampal slices, T-currents were found in 72% of the patches and found to have single channel conductances of 8 pS (Johnston et al. 1992,
397	In cilia; K 0.5 for Ca activation is 5 uM; most of Ca activated current is carried by chloride and persists in the absence of Na and K; Cl channel inhibitor 3',5-dichlorodiphenylamine-2-carboxylate (300uM) reduces current 90%; other Cl-channel inhibitors were tested [SITS, DIDS, A9C, DPC, NPPB, DCDPC]
398	In contrast, a study using radioactive in situ hybridization histochemistry looked at mRNA coding an NMDA glutamate binding protein and at NMDAR1 (an NMDAR subunit) expression and found heavy labeling for both in the pyramidal and polymorphic layers but little in the molecular layer
399	In gold fish retinal bipolar cells, four currents are observed: Ca currents, voltage- and calcium-dependent K currents, and Ih current
400	In mouse retinal bipolar cells, T-type Ca currents were recorded in soma, while L-type currents were recorded from axonal terminal
401	In mouse retinal bipolar cells, T-type Ca currents were recorded in soma, while L-type currents were recorded from axonal terminal
402	In patch recordings, "HVA-l channels reminiscent of L-type channels were occasionally encountered primarily in the more proximal dendrites" (and in the soma)
403	In PLTS cells “influx of Ca2+, while persistent depolarizations were due to influx of Na+. ”
404	In primary culture, GABA and glycine exert inhibitory actions on olfactory bulb neurons, mitral/tufted cells, granule and periglomerular cells
405	In retinal bipolar cells of bullfrog, both axon terminals and dendrites showed high GABA sensitivity mediated by both GABA(A) and GABA(C) receptors. GABA(A) and GABA(C) receptors may play different roles in the outer and inner retina and the differential complements of the two receptors on OFF and ON BCs may be closely related to physiological functions of these cells
406	In Salamander
407	In situ hybridization of three cloned SK channel subunits (SK1-3), the prime candidates likely to underlie Ca(2+)-dependent AHPs showed high levels of expression in regions presenting prominent AHP currents including CA1-3 regions of the hippocampus (SK1 and SK2), reticularis thalami (SK1 and SK2), supraoptic nucleus (SK3), and inferior olivary nucleus (SK2 and SK3)
408	In situ hybridization of three cloned SK channel subunits (SK1-3), the prime candidates likely to underlie Ca(2+)-dependent AHPs showed high levels of expression in regions presenting prominent AHP currents including CA1-3 regions of the hippocampus (SK1 and SK2), reticularis thalami (SK1 and SK2), supraoptic nucleus (SK3), and inferior olivary nucleus (SK2 and SK3)
409	In slices of rat brain at various postnatal ages was found that decay times of evoked IPSCs and spontaneous miniature IPSCs undergo progressive shortening during the first postnatal month
410	In slices that preserve mossy-fiber to granule cell synapses, Ach induced diverse responses in granule cells, one response being somatic current (nAChR also mediated postsynaptic currents, PSCs, which, however, were glutamatergic in nature, indicating a presynaptic mechanism. )
411	in SOBIV 297.
412	In the dorsolateral striatum, only parvalbumin mRNA-positive neurons expressed the mRNA encoding the potassium channel Kv3.1, a member of the Shaw family of potassium channels with rapid activation and inactivation kinetics, usually found in fast-firing neurons such as the basket cells of the hippocampus.”
413	In the hair-cell microvilli
414	In the hair-cell microvilli (Hudspeth AJ, Corey DP, others)
415	In triads made up of (i) a cholinergic axon, (ii) one or several periglomerular or granule cell dendrites, and (iii) usually one relay cell dendrite, asymmetric cholinergic synapses were selectively focused on dendrites (gemmules and spines) of periglomerular or granule cells.
416	In vitro, however, blocade of AMPA, NMDA, GABAA,D1 , D2, muscarinic receptors affect little the firing frequencies and patterns of cholinergic interneurons, indicating that these neurons are endogenously active and generate action potentials in the absence of any synaptic input
417	In vivo, the excitatory influence of STN contributes to the tonic discharge of SNr cells as shown by the marked reduction in SNr firing rate induced by a pharmacological blockade of STN activity
418	Inactivation of dendritic Na channel contributes to the attenuation of activity-dependent backpropagation of APs
419	Increased conductance may follow Ca impulses
420	Increased conductance may follow Ca impulses (Llinas and Walton 1998).
421	indicating that Ia synapses are distributed widely over soma-dendrites (confirmed by HRP labelling of Ia afferents on labelled motoneurones: reviewed in
422	Indirect evidence for this current was found in O-A interneurons
423	Indirect experimental evidence for dendritic Na channels was suggested by laminar filed potential studies
424	Individual branches can function as single integrative compartments where the fast oblique spike contains contributions from NMDA, VGCCs, and the A current
425	inferred
426	Inferred in
427	Inhibition of deep neurons (pyramidal and multipolar) by (presumed?) deep layer interneurons involves a fast Chloride and a slow potassium-mediated IPSP
428	Inhibitory interneurons, recorded mostly in the deeper part of layer II of piriform cortex, mediate fast IPSPs in principal cells and are activated at least partly through the axon collaterals of the principal cells
429	Input from dopaminergic neurons in the substantia nigra; causes small depolarization? sometimes a decrease in firing rate; modulates anomalous rectification of dendritic membrane (I IR)?
430	Intracellular recording from CA3 pyramidal neurons in a slice culture from rat found a slow excitatory response to Glu application in the presence of blocking agents for the ionotropic GluRs. Further experimentation revealed that ACPD could evoke the same response, which was due to the depression of I(K, Ca) and voltage-gated I(K)
431	Intracellular recording from CA3 pyramidal neurons in a slice culture from rat found a slow excitatory response to Glu application in the presence of blocking agents for the ionotropic GluRs. Further experimentation revealed that ACPD could evoke the same response, which was due to the depression of I(K,Ca) and voltage-gated I(K)
432	Intracellular recording from organotypic rat hippocampal cultures have shown that approximately 25% of single spikes in CA3 pyramidal neurons are followed by IPSPs at a fixed latency, presumeably a result of feedback inhibition from inhibitory interneurons. The addition of bicuculline (a competitive GABA(A) antagonist) completely abolished these responses, but they were insensitive to CGP35348, a GABA(B) antagonist
433	Intracellular recordings from sensorimotor cortex suggested that what activate IKCa persistently would not be calcium but some biochemical modification triggered by NMDA receptor activation
434	Intracellular recordings showed that Apamin-sensitive IKCa regulate pacemaker activity in these neurons
435	Intracellular recordings suggested different functional consequences for modulation of Ca2+ current subtypes. Based on the effects of specific organic Ca2+ channel blockers the sAHP was found to be coupled to N-, P-, and Q-type currents. P-type currents were coupled to the mAHP
436	Intracellular recordings: activation by I AHP causes unstable depolarizing plateau potentials; activated and modulated by 5-HT for decending raphe axons
437	Intracellular recordings: afterhyperpolarization potential inverses during repetitive impulse firing, limiting durations and frequency range of impulse firing
438	Intracellular recordings: AP5 blocks late component of EPSP elicited by olfactory nerve volley
439	Intracellular recordings: AP5 blocks late component of EPSP response to olfactory nerve volley
440	Intracellular recordings: AP5 blocks late component of EPSP response to olfactory nerve. volley
441	Intracellular recordings: AP5 blocks late component of EPSP response to olfactory nerve. volley
442	Intracellular recordings: CMQX and NBQX applied at the soma completely block short duration (i.e. near soma) single fiber EPSPs
443	Intracellular recordings: CNQX blocks early component of EPSP elicited by olfactory nerve volley
444	Intracellular recordings: CNQX blocks early component of EPSP elicited by olfactory nerve volley nerve volley
445	Intracellular recordings: CNQX blocks early component of EPSP response to olfactory nerve volley
446	Intracellular recordings: IPSP blocked by bicuculline and low Cl-
447	Intradendritic recordings show Ca-dependent plateau potentials and Ca impulses
448	Intrastriatal stimulation-induced release of ACh from presynaptic nerves hyperpolarizes cholinergic interneurons by activating muscarinic receptors (probably M2) located on somatodendritic region
449	Involvement of presynaptic NMDA receptors in cerebellar long-term depression at parallel fiber-Purkinje cell synapses
450	Ionophoretic glutamate applied to dendrites depolarizes Purkinje cells. Glu is released from parallel fibers of granule cells
451	IP3 gated ion channel; found in soma by
452	IPSP blocked by bicuculline
453	IPSP blocked by bicuculline and low Cl-
454	IPSPs elicited by monoamines in pyramidal cells result from a convergence of inputs from populations of layer II/III interneurons that are activated by one, two or all three of the following monoamines 5-HT, NE, and DA.
455	Isolated rod-dominant on-center bipolar cells respond to GABA, the highest sensitivity of which being located at the axon terminal
456	It contributes to the spontaneous activity of these cells and to the tonic inhibition of CA1 pyramidal neurons in the hippocampus
457	It has also been found that CNQX does not block the intracellular calcium concentration increase normally associated with stratum lucidum stimulation
458	It has also been found that CNQX does not block the intracellular calcium concentration increase normally associated with stratum lucidum stimulation
459	It has also been shown (using whole and perforated patch recording from acutely isolated CA3 pyramidal neurons) that application of Glu and quisqualatic acid (in the presence of D-AP5, an NMDAR-antagonist, and CNQX, an AMPAR antagonist) results in responses that consist of an inward current that may be preceded by an outward current. Both of these currents are affected by bath [K] and they had different pharmacological properties (Harata et al, 1996).
460	It has also been shown (using whole cell and perforated patch recording from acutely isolated CA3 pyramidal neurons) that application of Glu and quisqualatic acid (in the presence of D-AP5, an NMDAR-antagonist, and CNQX, an AMPAR antagonist) results in responses that consist of an inward current that may be preceded by an outward current. Both of these currents are affected by bath [K] and they had different pharmacological properties (Harata et al. 1996 #8680866).
461	It has been shown that activation of these receptors could facilitate transmitter release. Their activation is very fast (<10 ms) and lasts for seconds, and could contribute to the short-term plasticity characteristics of mossy fiber synapses
462	it has been shown to occur at mossy fiber synapses even in the presence of NMDA receptor antagonists under certain conditions
463	It has been suggested in rats that GABA(B) receptors modulate dendrodendritic inhibition primarily by inhibiting granule cell calcium channels and reducing the release of GABA
464	It has been suggested that the pharmacologically separable components of the HVA current in these neurons do not differ significantly in kinetics
465	It has been suggested that this current is not involved in the generation of AHP but (with other HVA currents) contributes to the inward currents that regulate interspike intervals during repetitive firing
466	It has been suggested that voltage-gated calcium channels play a role in LTP
467	It has been suggested that voltage-gated calcium channels play a role in LTP (Johnston et al. 1992), and it has been shown that nimodipine (an L-channel antagonist) prevents certain mossy fiber LTP-types from taking place
468	It was decreased by cannabinoids
469	It was shown that stimulation of PG cells results in self-inhibition: release of GABA from an individual PG cell activates GABA(A) receptors on the same neuron
470	It was was blocked by linopirdine in a reversible, concentration-dependent manner
471	Kinetic properties were studied using the whole-cell patch-clamp technique
472	Kinetic, pharmacological, and structural properties of these receptors were studied using patch-clamp techniques and single-cell reverse transcriptase polymerase chain reaction
473	Korf et al, 1976; Cheramy et al 1981) by backpropagating impulse
474	L-type ICa was found only in cells that retained axon terminals ramifying in the inner plexiform layer
475	Labeling for glutamic acid decarboxylase (GAD), the enzyme that synthesizes GABA, is heavy in the molecular layer of CA1
476	Large EPSPs activate I IR, increasing the membrane resistance, shortening the dendrites electrotonically, making the cell more sensitive to subsequent inputs (see
477	Lateral circuits contribute to the inhibitory surround. The bipolar neurons release glycine or GABA onto presynaptic bipolar neurons and ganglion cell dendrites
478	Layer 2/3 fast-spiking interneurons (most of which are basket cells) received the strongest excitatory input (presumably glutamatergic) from layer 4
479	Layer 4 basket cells in cat visual cortex receive asymmetric synapses from layer 6 pyramidal (~43%), the spiny stellate (44%) and thalamic afferents (13%)
480	Layer 4 basket cells in cat visual cortex receive excitatory input from neighboring spiny neurons, resulting in large excitatory EPSPs. One third of spiny cell-smooth cell pair were connected reciprocally (postsynaptic targets include local spiny stellate, pyramidal cells, as well as smooth neurons), but the postsynaptic IPSPs evoked by basket cells are slower, GABAergic, probably of GABAA type
481	Layer Ia horizontal cells receive a very small number of symmetrical synapses (presumably GABAergic?), in contrast to interneurons of the deeper layers of the piriform cortex -- globular, multipolar cells
482	Layer-4 basket cell axons make lateral connection isotropically near cell body ( 50 microm radius), but beyond this core region, anisotropically, preferably within a particular angular sectors cell body
483	Leads to a fast EPSP which allows an influx of cations. This can work with the M1 receptors to switch the cell from burst to tonic mode
484	lighter staining for GABA/GAD; SOBiv p132). Cartwheel cells produce IPSPs in pyramidal cells (see
485	Llinas and Walton 1990).
486	low density
487	Low threshold calcium spikes were antagonized by T-channel blockers in rat
488	Low threshold inactivating Ca2+ current
489	Low-voltage-activated (LVA) and high-voltage-activated (HVA) Ca2+ currents were observed in the isolated rod bipolar cell terminal recordings
490	Macropatch clamp and intracellular recordings in guinea pigs suggested that the pattern of Ca2+ spike firing in the dendrites of Purkinje cells is dynamically modulated by a highly aminopyridine-sensitive K+ current, and probably also by a Ca2+-activated potassium current
491	Mammal. (See SOBiv p140).
492	Many amacrine-to-ganglion cell synapses accumulate glycine
493	Many authors have described the activation of dendritic voltage activated Ca channels
494	Matsui K, Hosoi N and Tachibana M, 1998
495	May generate long delays contributing to temporal patterns (Ketchum and Haberly 1991); may play a role in epileptogenesis
496	Mechanisms underlying suppression of this current by odorants were investigated in newt ORNs using the whole-cell version of the patch-clamp technique
497	Membrane patches recorded in the cell-attached patch configuration from the soma and apical dendrites revealed an Ih that increased over sixfold from soma to distal dendrites. Ih demonstrated a mixed Na+-K+ conductance and was sensitive to low concentrations of external CsCl. As a result of Ih the propagation of subthreshold voltage transients is directionally specific.The elevated dendritic Ih density decreases EPSP amplitude and duration and reduces the time window over which temporal summation takes place
498	mGluR2 knockout mice show normal LTP and synaptic transmission but not LTD
499	Microionophoretic studies
500	Mitral-cell soma-dendrites act as a presynaptic terminal to the granule cell; the circuit is recurrent onto the injected cell; and the inhibitory transmitter is GABA
501	MK801 (an NMDAR antagonist) blocks the transient intracellular Ca2+ release normally associated with stratum lucidum stimulation (found by simultaneous Ca imaging and intracellular recording in rat brain slices by
502	Modulation of synaptic transmission between granule cells and Purkinje cells via presynaptic GABAB receptors
503	Modulation of this current by dopamine was studied using standard patch-clamp techniques.
504	Morphological evidence of local contact by pyramidal neurons
505	Mose retinal ganglion
506	Most layer 2/3 pyramidal neurons and interneurons received inhibitory input (presumably GABAergic) from neighboring interneurons in layer 2/3
507	Mouse
508	mRNA of A-channel subunit Kv4.2 is expressed predominantly in granule cells. (In contrast, that of Kv4.3, also of A-channel, is expressed predominantly in periglomerular cells)
509	mRNA of A-channel subunit Kv4.2 is expressed predominantly in granule cells. (In contrast, that of Kv4.3, also of A-channel, is expressed predominantly in periglomerular cells)
510	mRNA of A-channel subunit Kv4.3 is expressed predominantly in periglomerular cells. (In contrast, that of Kv4.2, also of A-channel, is expressed predominantly in granule cells)
511	N-type Ca2+ currents in rat neostriatal cholinergic interneurons is reduced through D2 receptor activity
512	Na action potentials support backpropagating impulses
513	Na impulses may underly "fast prepotentials" that boost distal EPSPs
514	NaV1.1 is present in the soma and proximal dendrites, NaV1.6 is robustly present in cell bodies and dendrites, and NaV1.7 is absent from the cell
515	NaV1.2 is substantially present throughout the dendrites, NaV1.1 is present in the soma and proximal dendrites, NaV1.6 is robustly present in cell bodies and dendrites, and NaV1.7 is absent from the cell
516	Neostriatal cholinergic interneurons fire irregularly but tonically in vivo. The summation of relatively few depolarizing potentials and their temporal sequence are thought to underlie spike triggering and the irregularity of action potential timing, respectively
517	Nitric oxide, released from both mitral and granule cells, is involved in olfactory memories and may act as a retrograde and/or intracellular messenger. However, only mitral cells expressed guanylyl cyclase subunits.
518	NMDA and AMPA conductances properties were studied using patch-clamp recordings in morphologically identified cells in slices prepared from surgically removed medial temporal lobe specimens of epileptic patients (14 specimens from 14 patients
519	NMDA and AMPA conductances properties were studied using patch-clamp recordings in morphologically identified cells in slices prepared from surgically removed medial temporal lobe specimens of epileptic patients (14 specimens from 14 patients). The wide range of changes in the slope conductance of the NMDA EPSCs suggests that the NMDA-receptor-mediated conductance could be altered in human epileptic DGCs
520	NMDA iontophoretically applied to basal dendrites evoked inward currents near resting potential. Changing levels of bath calcium concentration downwards by 50% caused an increase in the inward current
521	NMDA receptor is required for DDI (dendrodendritic inhibition) since IPSC was completely blocked by AP-5. Ineffectiveness of AMPA receptor-mediated EPSPs to activate the granule cells may be due to their intrinsic membrane properties.
522	NMDA receptors play a critical role in dendrodendritic inhibition between mitral and granule cells. Moreover, N- and P/Q type calcium channels are involved.
523	NMDA reversibly depresses postsynaptic currents, through a trans-synaptic mechanism that involves release from parallel fibers nitric oxide that decreases the glutamate sensitivity of the Purkinje cell
524	Nomarski optics and infrared videomicroscopy were used to demonstrate the existence of a TTX-sensitive persistent Na+ conductance (INaP) in identified medium-sized neostriatal neurons
525	Nucleated patches revealed a fast component highly sensitive to external 4-AP and TEA (~57% of total K+ current) and a slow component that was sensitive to high concentrations of TEA, but insensitive to 4-AP (~25% of total K+ current)
526	Numerous authors (e.g.,
527	ON beta Ganglion cells. ON beta Ganglion cells respond to ionophoresed GLU and GLU agonists, and are blocked by GLU antagonists (SOBiv p238). Ganglion cells express GLUR and NMDAR
528	on spines (SOBiv p126,130). The neurotransmitter is GLU
529	One STN regulator is the serotonin (5-HT) system. The STN receives a dense 5-HT innervation. 5-HT1A, 5-HT1B, 5-HT2C, and 5-HT4 receptors are expressed in the STN. 5-HT may regulate the STN via several mechanisms."
530	Original intracellular recordings in vivo
531	P)
532	P2
533	p395).
534	p396
535	p396).
536	p396.
537	p397).
538	p397.
539	Paired recordings in slices showed excitatory transmission mediated solely by transmitter spillover between mitral cells. Dendritic glutamate release causes self-excitation via local activation of NMDA receptors, and generates NMDA receptor-mediated responses in neighbouring cells. It is suggested that this simultaneous activation of neighbouring cells by a diffuse action of glutamate provides a mechanism for synchronizing olfactory principal cells
540	Paired whole-cell recording revealed reciprocal excitatory connections between mitral cells. Pharmacological analysis suggested that it could be mediated by both AMPA and NMDA receptors
541	Patch Clamp recordings revealed density levels are similar to that found in the soma, with slightly different kinetics
542	Patch recordings
543	Patch recordings indicate channels similar in basic characteristics to one or more of the HVAm channel types (most likely Q- or R-type channels)
544	Patch recordings of back propagating impulses in dendrites. Variable densities of active channels support variable extents of backpropagating impulse in the dendrites
545	Patch recordings yield an approximate channel density of 28 pS/micron^2 in juvenile rats < 4 wks of age, rising to 61 pS/micron^2 in older rats. Channel density was similar in other dendritic compartments
546	Patch recordings yield an approximate channel density of 45 pS/micron^2 (compared with 28 pS/micron^2 in dendrites) in juvenile rats < 4 wks of age, rising modestly to 56 pS/micron^2 (compared with 61 pS/micron^2 in dendrites) in older rats
547	Patch recordings yield an approximate channel density of 7 pS/micron^2 in juvenile rats < 4 wks of age, rising to 10 pS/micron^2 in older rats. Ca channel density was similar in other dendritic compartments, and in general lower than Na channel density
548	Patch recordings yield an approximate channel density of 7 pS/micron^2 in juvenile rats < 4 wks of age, rising to 10 pS/micron^2 in older rats. Ca channel density was similar in other dendritic compartments, and in general lower than Na channel density
549	Patch-clamp recordings from human cells showed N-type, L-type and T-type currents that had similar pharmacological and kinetic characteristics as in control rats. The current density was significantly larger in human and in the kainate model compared to cells isolated from adult control rats
550	Patch-clamp recordings reveal a high density of A-type K channels in the dendritic tree, which increases with distance from the soma
551	Patch-clamp recordings reveal A-type K channels in the soma
552	Patch-pipette recordings found no evidence for a ?sag? in hyperpolarizing responses, suggesting that this current is not present in these neurons
553	Perforated whole-cell voltage-clamp recordings showed that dopamine modulates the L-type Ca2+ channels in rat olfactory receptor neurons via a voltage-independent mechanism
554	Perhaps the principal function of these neurons is to release SOM, NOS, and/or NPY, all of which could exert slower neuromodulatory effects on their postsynaptic targets rather than fast synaptic effects. For example, SOM has been shown to exert a potent presynaptic inhibition on GABA release at SPN–SPN synapses.”
555	Perhaps the principal function of these neurons is to release SOM, NOS, and/or NPY, all of which could exert slower neuromodulatory effects on their postsynaptic targets rather than fast synaptic effects. For example, SOM has been shown to exert a potent presynaptic inhibition on GABA release at SPN–SPN synapses.”
556	Periglomerular cells respond to microapplication of GABA, acetylcholine, norepinephrine and glycine with the activation of distinct ionic currents.
557	PG cells closely resembled previously described periglomerular cells in their morphology. During current clamp recording these neurons were characterized by their lack of action potentials upon depolarization. Consistent with these results no Na+ currents could be elicited in voltage clamp experiments. Two types of outward K+ currents were distinguished: one which inactivated and one which did not.
558	PKC may have a negative feedback role in modulating excitation by 5-HT in piriform cortical interneurons
559	PLTS cells exhibited unique firing properties due to Ca*+-dependent low-threshold spikes and Na+-dependent persistent depolarized spikes, in addition to Na+-dependent fast spikes.”
560	PLTS interneurons receive numerous synaptic contacts on their proximal dendrites from both cholinergic and dopaminergic axons, as well as onto their distal dendrites, which receive asymmetric synaptic inputs from the cortex.”
561	PLTS interneurons receive numerous synaptic contacts on their proximal dendrites from both cholinergic and dopaminergic axons, as well as onto their distal dendrites, which receive asymmetric synaptic inputs from the cortex.”
562	PLTS interneurons were found to evoke only sparse and relatively weak GABAergic IPSCs in SPNs.”
563	Possible
564	Potassium-induced glutamate release from granule cells is dependent on the entry of Ca++ through multiple types of Ca-channel including N-, L-, P/Q-types; a number of these channel subtypes seems to be involved in the presynaptic modulation, by GABAB receptors, of potassium-induced glutamate release
565	Potentiation of intrinsic excitability was induced by relatively weaker inputs than those that induce potentiation of synaptic efficacy; NMDA receptors are involved in both aspects of potentiation
566	pp385,389,393-395,407).
567	Presence of Kv4.2 but not Kv1.4 subunits in the somatodendritic membrane. Depolarization-activated potassium currents in cholinergic interneurons were dominated by a rapidly inactivating, K+-selective A current that became active at subthreshold potentials.
568	Presence of Kv4.2 but not Kv1.4 subunits in the somatodendritic membrane. Depolarization-activated potassium currents in cholinergic interneurons were dominated by a rapidly inactivating, K+-selective A current that became active at subthreshold potentials
569	Presence of Kv4.2 but not Kv1.4 subunits in the somatodendritic membrane. Depolarization-activated potassium currents in cholinergic interneurons were dominated by a rapidly inactivating, K+-selective A current that became active at subthreshold potentials
570	Presence of Subthreshold-operating transient (A-type) K(+) currents (I(SA)s), as indicated by an accesspry subunit that accelerates the kinetics of this current
571	Present in lower density than in the cilia
572	Present in lower density than in the cilia.Properties of this channel in rat, and its functional interplay with the CNG channel, were studied by using inside-out membrane patches excised from ORN dendritic knobs/cilia
573	presumably GABA inhibition (summarized in Young and Oertel,
574	presumed
575	Presynaptic terminal and axon NMDAR's have been found withimmunocytochemical techniques
576	Probably.
577	Prolongation of ISI through a D1 dopamine receptor-mediated enhancement of the afterhyperpolarization (AHP)
578	Properties of K+ outward currents were investigated in human DG cells from 11 specimens obtained from patients with temporal lobe epilepsy. An IK was observed in all cells. The average current density, the time-dependent decay, and the resting membrane characteristics were not significantly different between patients with and without Ammon Horn Sclerosis. The V1/2(inact) was shifted in a hyperpolarizing direction in AHS (-67.7mV) compared with that in hippocampi not showing AHS (-47.7mV)
579	Properties of potassium outward currents were investigated from 11 specimens obtained from patients with temporal lobe epilepsy. An IK but not IA or inwardly rectifying potassium currents, were observed in all cells
580	Properties of this channel in rat, and its functional interplay with the CNG channel, were studied by using inside-out membrane patches excised from ORN dendritic knobs/cilia
581	Properties of this current and its modulation by PKA were studied using whole-cell patch-clamp recording techniques
582	provide evidence that activation of these receptors is necessary for LTP induction
583	provide evidence that activation of these receptors is necessary for LTP induction .
584	Quantitative autoradiography has been used to localize [3H]AMPA binding sites. In CA3, labeling was substantially heavier in s. pyramidale than in s.radiatum and s. lacunosum-moleculare
585	Quantitative autoradiography has been used to localize [3H]AMPA binding sites. It was found that AMPARs are found in a high concentration in the hippocampus relative to other areas in the brain. In CA3, labeling was substantially heavier in s. pyramidale than in s.radiatum and s. lacunosum-moleculare
586	Quantitative autoradiography has been used to localize sites at which L-[3H]-glutamate is displaced by NMDA. The labelling of these receptors was somewhat lower than in CA1 overall, being highest in s. oriens and s. radiatum and very low in s.pyramidale and s. lucidum
587	quote from the review in Llinas and Walton 1990).
588	Rat
589	Re: PG cells: Two types of outward K+ currents were distinguished: one which inactivated and one which did not.
590	Recording from dissociated neurons using intracellular and whole-cell voltage-clamp recordings showed that carbachol can act at M1-like muscarinic receptors to reduce the membrane K+ conductances and excite the neostriatal neurons
591	Recordings from acute brain slices and in anesthetized rats using whole-cell recordings and Ca2+ imaging found that backpropagation of action potentials into the dendritic arbor is actively supported by Na+ channels both in vitro and in vivo.
592	Recordings from acute brain slices and in anesthetized rats using whole-cell recordings and Ca2+ imaging found that single action potentials evoke little or none Ca2+ influx in the dendritic tuft, unless is paired with synaptic input
593	Recordings from acute brain slices and in anesthetized rats using whole-cell recordings and Ca2+ imaging found that single action potentials evoke substantial Ca2+ influx in the apical trunk.
594	Recordings from membrane patches of dendrites and soma reveal fast and slow responses to fast application of glutamate, mediated by AMPA amd NMDA receptors, respectively
595	Recordings from membrane patches of dendrites and soma reveal fast and slow responses to fast application of glutamate, mediated by AMPA and NMDA receptors, respectively
596	Recordings in slices showed that D1 receptor activation can either inhibit or enhance evoked activity, depending on the level of membrane depolarization, by modulating an L-type Ca2+ conductance
597	Recordings in slices showed that GABA inhibition was mediated by GABA(B) receptors in the dendrites and GABA(A) receptors in the soma and dendrites
598	Recordings using infrared-guided laser stimulation combined with whole cell recordings revealed a highly nonuniform distribution. Hot spots, with amplitude and integral of glutamate-evoked responses three times larger than responses evoked at neighboring sites, were detected. It appeared that the larger responses evoked resulted from an increase in activation of both AMPA and NMDA receptors. There was no correlation with branch points
599	Recordings using the intracellular perfusion method showed no differences between the I-V characteristics of CA1 and CA3 neurones for this current. In contrast to this, the steady-state inactivation of both types of neurones was significantly different
600	report the presence and function of Ih.
601	Response of isolated bipolar cells to glycine
602	Response to glutamate in isolated bipolar cells
603	Reversed chloride gradients, demonstrated by cytochemical methods, may be responsible for excitatory GABA effects on selected periglomerular neurons
604	reviewed by
605	Reviewed in
606	reviewed in
607	Reviewed in
608	reviewed in
609	reviewed in
610	Reviewed in
611	Reviewed in
612	Reviewed in
613	reviewed in Haberly 1998).
614	reviewed in Llinas and Walton, 1990).
615	reviewed in McCormick 1998).
616	reviewed in Shepherd 1998). Variable densities of active channels support variable extents of backpropagating impulse in the dendrites
617	Rhodopsin (rods) and red, green and blue opsins (cones), in disc membranes of the distal segment.
618	Rhodopsin (rods) in disc membranes of the distal segment.
619	see also
620	see also
621	see also
622	see also
623	see also Felix and MacLennan, 1971).
624	see also Tseng and Haberly 1989b; reviewed in
625	see Burke 1998 for references). Single-fiber Ia EPSPs have widely varying shapes
626	See SOBiv p140).
627	Selective localization of GABA receptors at symmetric synapses ( and of gluR at asymmetric synapses.)
628	Sensitive to TTX. This generates the impulses that propagate into the axon
629	Sensitive to TTX. This plateau potential underlies impulse bursting
630	Serotonin produced a slowly developing and long-lasting suppression of IM leading to depolarization end excitation
631	Sherman and Koch, 1990).Using electrophysiological recordings and imaging, the density of these channels was found to rapidly decrease with distance from soma and clustered in high density around the base of dendrites
632	showed that the proximal dendrites and somata of hippocampal neurons label for L-type Ca2+ channels and that these channels tend to cluster near the bases of the neural processes. In patch recordings, "HVA-l channels reminiscent of L-type channels were occasionally encountered primarily in the more proximal dendrites" (and in the soma)
633	Silent synapses during development
634	Simultaneous recordings were carried out in visual cortical slices. Assuming open probability of non-NMDA receptor channels to be 0.7, it is suggested that the number of channels available for synaptic transmission between individual pyramidal cells would be 74 (kittens) and 59 (rats)
635	Simultaneous whole-cell recordings, made from the soma and dendrites rat brain slices, showed that AP evoked by either current pulses or synaptic stimulation of parallel or climbing fibers, always occurred first at the soma and decreased in amplitude with increasing distance into the dendrites. Simultaneous somatic and axonal recordings showed that these action potentials were initiated in the axon
636	Simultaneous whole-cell recordings, made from the soma and dendrites rat brain slices, showed that AP evoked by either current pulses or synaptic stimulation of parallel or climbing fibers, always occurred first at the soma and decreased in amplitude with increasing distance into the dendrites. Simultaneous somatic and axonal recordings showed that these action potentials were initiated in the axon. Outside-out patches excised from the soma and dendrites up to about 100um revealed a channel density decreasing with distance from the soma.
637	Single action potential backpropagations show dichotomy of either strong attenuation (26-42%) or weak attenuation (71-87%). The dichotomy seems to be conferred primarily by differences in distribution, density, etc. of voltage dependent sodium and potassium channel (A-type, especially ) along the somatodendritic axis
638	single fiber EPSPs:
639	Single unit extracellular recordings showed a short latency GABAA inhibition that arises from the axon collaterals of pars reticulata projection neurons
640	Single-cell-reverse transcription-polymerase chain reaction analysis of glycine receptor-subunit expression was combined with whole-cell recordings from acutely isolated cholinergic interneurons. Subunits alpha2, beta, alpha3, were found to be associated with receptor properties such as efficacy and desensiutization. Celllular localization of receptors unclear, but presumably on soma (?)
641	Single-channel and whole-cell recording identified three types of current: a transient inward sodium current and a transient and a sustained outward potassium current
642	Single-channel recordings from inside-out membrane patches excised from toad chemosensory cilia showed the presence of 4 different types of KCa channels, with unitary conductances of 210, 60, 12, and 29 and 60 pS, high K+-selectivity, and Ca2+ sensitivities in the low micromolar range
643	Single-fiber Ia EPSPs have widely varying shapes
644	Slow inactivation of sodium channels in dendrites and soma will modulate neuronal excitability in a way that depends in a complicated manner on the resting potential and previous history of action potential firing
645	Slow second messeger pathway that leads to a reduction in K+ current. This can switch the cell from burst to tonic mode
646	SNr GABA neurons express a strong Kv3-like current with fast activation and slow inactivation kinetics that is required for the sustained high frequency firing capability in these neurons"
647	SNr neurons contain both muscarinic
648	sobiv 242). This is excitatory
649	sobiv 242). Dendritic compartments not specified.
650	SOBiv p128). Granule cells are similar to cerebellar granule cells (SOBiv p132).
651	SOBiv p131).
652	SOBiv p140). Such sequences are seen after acoustic stimulus
653	SOBiv p140).(P1)
654	sobiv p217)
655	sobiv p217), boosting ganglion cell transients, increasing sensitivity to motion
656	sobiv p217). These nicotinic receptors desensitize rapidly
657	SOBiv p238). Multiple subunits of GLUR and NMDAR are present
658	SOBiv p238). Some bipolar cells contain glycine
659	SOBiv p238).Clusters of glycine receptors were found on the somatodendritic membranes of Alpha ganglion cells
660	SOBiv p243).
661	SOBIV p316
662	SOBIV p316).A study indicates that synaptic activation of these receptors increases inhibitory activity in relay neurons by increasing output of presynaptic dendrites
663	SOBIV p317).
664	SOBiv p88). Glutamate is released from Ia terminals
665	SOBiv p91.
666	SOBiv p94). Glycine ionophoresis mimics Ia IPSPs (reviewed by
667	SOBiv p94). Ia IPSPs are blocked by strychnine, a known blocker of Glycine receptors (SOBiv p94).
668	SOBiv p95.
669	SOBiv p96).
670	Soma and proximal apical dendrites receive mainly flattened (FL) or pleiomorphic (PL) vesicle synapses on their trunks. These are correlated with IPSPs (SOBiv p128,130-1). Cartwheel cells stain for CLY
671	Somatic and Dendritic patch recordings showed an even density of Na channels (120pSum-2) up to 350 um from the soma along the primary dendrite to theorigin of the glomerular tuft
672	Some diferences in the neurons in the deeper layers (v.s. those in the superficial layers) can be accounted for by differences in the IA channel in the cells
673	Some kinetic properties of this current were studied in cell-attached recordings in rats
674	Spike-triggered calcium entry shaped the falling phase of the action potential waveform and activated calcium-dependent potassium channels
675	Spontaneous and electrically driven GABAergic synaptic inputs to PG cells come possibly from other interneurons in the glomerular layer.
676	Spontaneous firing was driven by the combined action of a sodium current and the hyperpolarization-activated cation current (I(h)), which together ensured that there was no zero current point in the subthreshold voltage range. Spike-triggered calcium entry shaped the falling phase of the action potential waveform and activated calcium-dependent potassium channels
677	spontaneously released dopamine from dopamine dendrites induces tonic activation of D1-like receptors and exerts a tonic excitatory influence on SNr GABA neurons"
678	spontaneously released dopamine from dopamine dendrites induces tonic activation of D1-like receptors and exerts a tonic excitatory influence on SNr GABA neurons."
679	Starburst amacrine cells release a pulse of Ach onto ganglion cells dendrites
680	Steady-state inactivation curve is 10 mV more depolarized in SP cells in endopiriform nucleus. "Modelling analysis suggested that this difference is sufficient to explain the more depolarized membrane potential of deep cells, and results in a 2-fold decrease in latancy of the first spike evoked by depolarizing steps"
681	STN neurons containing a4ß2 nAChRs (a4ß2 neurons) received more glutamatergic inputs, and preferentially innervated GABAergic neurons in the substantia nigra pars reticulata. In contrast, STN neurons containing a7 nAChRs (a7 neurons) received more GABAergic inputs, and preferentially innervated dopaminergic neurons in the substantia nigra pars compacta."
682	Striatal FSIs make [GABAergic] synapses onto both direct and indirect path- way SPN. The biophysical properties of the synaptic contacts do not differ and exhibit short-term depression. Further, single FSI often make synapses with both types of SPN”
683	Strychnine-sensitive glycine receptors are present on a subpopulation of the cholinergic interneurons in rat caudatoputamen, supporting the hypothesis that (excitatory) glycine receptors inducing striatal release of [(3)H]acetylcholine may be localized to cholinergic neurons
684	Substantial in most deep pyramidal and multipolar cells; generates hyperpolarizing potentials lasting several seconds; as I AHP contributes to rapid spike frequency adaptation; blocked by cholinergic agonists
685	Subthalamic nucleus neurons make glutamatergic connections on neurons of the globus pallidus.
686	Subthalamic nucleus neurons receive input from GABAergic globus pallidus neurons through GABA-A receptors.
687	Subthreshold membrane potential oscillations are blocked by bath application of tetrodotoxin (TTX), a potent Na(t)-current antagonist, in rats 3-17 days old
688	Suggested.
689	suggesting the presence of mGluRs.
690	suggesting the presence of mGluRs.
691	Synapse of type 2
692	Synaptic inhibition of mitral cells: Yamamoto et al, 1962;
693	T-type calcium current recorded in bipolar cells in slice in mouse
694	T-type channels are less dense in the soma than in the dendrites
695	The A current increases with distance from the soma normalizes Ca+ signals during AP propagation
696	The action potential has a pronounced Ca component on its falling phase
697	The amplitude of ensemble K+ currents in cell-attached patches decreased along the apical dendrite as the distance from the soma increased, with a slope of -0.9 +/- 0.3 pA per 100um. In nucleated outside-out patches from soma in acute slices of sensorimotor cortex from 13- to 15-day-old Wistar rats some patches contained only I-A-like channels, other contained only IK-like channels that did not inactivate or inactivated slowly, and the remainder contained mixtures of both types. The amount of IA and IK depended weakly on distance along the primary apical dendrite from the soma. The amplitude of IA increased, while the amplitude of IK decreased
698	the back-propagating action potential may be important for the dendritic release of dopamine"
699	The balance between synaptic (glutamatergic) and non-synaptic conductance indicates that the synapse will not shunt the cell and the conductance ratio serves to maximize incremental gain at the photoreceptor to ON bipolar synapse.
700	The basal conductance of unstimulated frog ORN was investigated using whole-cell and perforated-patch recording. It was found that under physiological conditions, gating of CNG channels contributes approximately 0.06 nS to the resting neuronal conductance
701	The baskets formed by inhibitory basket cells have high concentrations of glutamic acid decarboxylase (GAD), the enzyme that synthesizes GABA
702	The CA1 oblique dendrites (also called radial oblique) are the main target of the Schaffer collaterals from CA3, and are therefore the primary sites of generation of LTP.
703	The cellular localization of GABAB binding was investigated using lesion techniques. It was suggested that the majority of cerebellar molecular layer GABAB binding sites are located on Purkinje cell dendrites. During development binding in the molecular layer peaks between postnatal day 14 and postnatal day 28 and then decreases to adult levels
704	The contribution of a fast (IAt), and a slowly (IAs)-inactivating A-currents were studied in slices. The results suggest a role for these currents to define the limits on the depolarized state
705	The contribution of an inwardly rectifying current (IKir) were studied in slices. The results suggest that the hyperpolarized state is determined principally by this current
706	The developmental evolution of Ca-dependent spikes in the tuft was investigated using simultaneous somatic and dendritic recordings
707	The distribution of GABAA and GABAB receptors was studied with patch-clamp recording in combination with infrared-guided laser stimulation to release GABA photolytically. The data suggest that relatively more GABAA receptors are located at the apical dendrite and relatively more GABAB receptors near the soma
708	The distribution of the P-type calcium channel in the mammalian central nervous system has been demonstrated immunohistochemically by using a polyclonal specific antibody. Electron microscopic localization revealed labeled patches of plasma membrane on the soma, main dendrites, spiny branchlets, and spines; portions of the smooth endoplasmic reticulum were also labeled. Strong labeling was present in the periglomerular cells of the olfactory bulb, ...etc
709	The effects of glutamate on SNr cells is mediated by the three principal types of glutamate receptors: a-amino 3hydroxy-5methyl- 4-isoxaline propionic acid/kainate (AMPA), N-methyl-D aspartate (NMDA) and metabotropic receptors [mGluR1 and mGluR5]” Reviewed in
710	The effects of glutamate on SNr cells is mediated by the three principal types of glutamate receptors: a-amino 3hydroxy-5methyl- 4-isoxaline propionic acid/kainate (AMPA), N-methyl-D aspartate (NMDA) and metabotropic receptors” Reviewed in
711	The effects of intracellular calcium buffering on electrical tuning were studied in hair cells at apical and basal cochlear locations tuned to 100 and 300 Hz. Ca2+ imaging revealed about twice as many hotspots of Ca2+ entry during depolarization in high-frequency compared to low-frequency hair cells. It is suggested that each KCa channel is gated by Ca2+ entry through a few nearby Ca2+ channels, and that Ca2+ and KCa channels occupy, at constant channel density, a greater fraction of the membrane area in high-frequency cells than in low-frequency cells
712	The effects of intracellular calcium buffering on electrical tuning were studied in hair cells at apical and basal cochlear locations tuned to 100 and 300 Hz. High conductance KCa channels were 2-fold less Ca2+ sensitive in high-frequency than in low-frequency cells. It is suggested that each KCa channel is gated by Ca2+ entry through a few nearby Ca2+ channels, and that Ca2+ and KCa channels occupy, at constant channel density, a greater fraction of the membrane area in high-frequency cells than in low-frequency cells
713	The effects of this current on the firing properties were studied in brainstem slices
714	The fast and slow components of EPSCs were studied using whole cell patch clamp recordings
715	The functional properties of AMPA receptors were studied in acute slices. It was found that AMPARs expressed in different types of basal ganglia neurons were markedly diverse
716	The functional properties of NMDA receptors were studied in acute slices. Little variability in functional properties was found in different types of basal ganglia neurons
717	The GABABR1a antibody selectively marked the neuropil in layer Ia, where afferent olfactory fibers and intrinsic GABAergic axons terminate on the distal apical dendrites of pyramidal neurons. GABABR1a may be involved in feedforward synaptic circuits
718	The globus pallidus, a neuronal nucleus involved in the control of motor behavior, expresses high levels of histamine H3 receptors (H3Rs) most likely located on the synaptic afferents to the nucleus.”
719	The GP is mainly made up by two populations of GABAergic neurons, with the predominant one projecting to the subthalamic nucleus while a second group sends projections to the striatum."
720	The kinetic properties of this current have been studied in mice using voltage clamp with whole-cell patch recordings
721	The kinetic properties of this current were studied in cell-attached recordings in rats
722	The kinetic properties of this current were studied using the whole-cell voltage-clamp method in acutely isolated cells. No significant differences were found after induction of status epilepticus
723	The kinetics of GABA currents were studied using flash photolysis of caged GABA
724	The kinetics properties of this current were studied using whole-cell recording from dissociated neurons. Unlike other cells, recovery from inactivation was accompanied by a sizeable ionic current. It was suggested that the current flowing during this recovery may depolarize the cells immediately after an AP, promoting the typical high-frequency firing of these neurons (complex spike)
725	The main synaptic afferents to GP are striato-pallidal GABAergic axons."
726	The mGluRs belonging to group I and II are located on the axon terminals of striatal cholinergic interneurons, their activation resulting in facilitation and inhibition, respectively, of acetylcholine release
727	The most characteristic attributes of these neurons were the presence of a low threshold Ca2+ spike."
728	The NMDA responses of two types of feedforward excitatory interneurons in the granular layer, the granule cell and unipolar brush cell (UBC), were compared. A subset of granule cells receive influence from UBC via extrinsic mossy fibers
729	The OFF cone bipolar cells seem dominated by glycinergic input and the ON cone bipolar and rod bipolar cells by GABAergic input
730	The oscillations and the intermittent firing pattern are Ca2+ or SK channel independent, but are completely eliminated by TTX, suggesting that they are due to an interaction between voltage-gated K+ conductances and a persistent or possibly the inactivating sodium conductance responsible for spike generation.”
731	The pharmacologically isolated, GABAergic synaptic currents in bipolar cells were long-lasting (compared with those in in ganglion cells, which are relatively brief). The GABAA receptor component of the bipolar cell response was relatively brief compared with the GABAC receptor component
732	The pharmacology and kinetics of glutamate sensitivity of mitral cells was studied using flash photolysis in rats
733	The physiology of these receptors has been studied in outside-out patches from the proximal apical dendrites. It was found that a CNQX-sensitive component of the synaptic current evoked by fast aplication of glutamate could be isolated (and was presumed to be the result of AMPA channel opening). It was calculated that AMPA channels had a mean elementary conductance of 10 pS (estimated by non-stationary fluctuation analysis) and was found that the channels had a low permeability to Ca2+. The reversal potential for AMPA receptors was found to be about 0 mV with an almost linear peak current-voltage relationship
734	The physiology of these receptors has been studied in outside-out patches from the proximal apical dendrites. It was found that an APV-sensitive component of the synaptic current evoked by fast aplication of glutamate could be isolated (and was presumed to be the result of NMDA channel opening). It was calculated that NMDA channels had a main conductance state conductance of 45 pS and it was confirmed that the channel was permeable to Ca2+. The NMDAR-mediated conductance was blocked by Mg2+ in a voltage-dependent way and by Zn2+ in a non-voltage-dependent fashion
735	The presence of L-channels in all dendritic compartments in mouse motoneurons is supported by electrophysiology and immunehistochemistry
736	The presence of Calcium channels was directly demonstrated by imaging studies
737	The presence of GABAB receptor subtypes BR1 and BR2 on the presynaptic and postsynaptic membranes of GABAergic striatonigral synapses and glutamatergic STN like terminals indicates that besides GABAA, GABAB receptors are also implicated in GABAergic striatonigral transmission."
738	The properties of outward currents were investigated with patch-clamp in acutely isolated cells at various postnatal ages and at adulthood (2-3 mo). Kinetic analysis and pharmacological properties showed that IK and IA were present in these cells. IA and IK remained stable with respect to kinetic properties during ontogenesis, but the relative contribution and pharmacological properties varied with age. IA dominated in P5-7 cells whereas IK was prominent in most older cells
739	The properties of outward currents were investigated with patch-clamp in acutely isolated rat DGCs at various postnatal ages and at adulthood (2-3 mo). Kinetic analysis and pharmacological properties showed that IK and IA were present in these cells. IA and IK remained stable with respect to kinetic properties during ontogenesis, but the relative contribution and pharmacological properties varied with age. IA dominated in P5-7 cells whereas IK was prominent in most older cells
740	The properties of this current have been studied in cell-attached recordings in rats
741	The properties of this current were studied using intracellular recording in slices
742	The properties of voltage-gated potassium currents were studied in acutely isolated rat cells from area CA1 and CA3 at postnatal ages of day 6-8, 9-14, and 26-29 (P6-8, P9-14, and P26-29) with the use of the whole cell version of the patch-clamp technique. In CA1 cells IK was blocked by TEA at +30 mV with an IC50 of 0.98 mM. In CA3 cells the corresponding IC50 value was 1.05 mM. About 20% of IK were insensitive to TEA. IK was partially blocked by approximately 30% with 100 microM 4-AP. Mast cell degranulating peptide (100-200 nM) and dendrotoxin (50-300 nM) had no effect on IK. IK was upregulated with increasing postnatal age. This increase in the expression of IK was approximately 300% much larger in CA1 cells than in CA3 cells, with only approximately 50%
743	The rate of NMDAR channel opening was studied in response to depolarisations at different times after brief (1 ms) and sustained (4.6 s) applications of glutamate to nucleated patches from neocortical pyramidal neurons
744	The responses of most retinal ganglion cells are transient because bipolar-to-ganglion cell transmission is truncated after 150 msec by a feedback inhibition to bipolar cell terminals from GABAergic amacrine cells; the feedback inhibition itself must be delayed by approximately 150 msec to allow the initial bipolar-ganglion cell transmission. One source of the delay appears to be glycinergic amacrine cells to GABAergic amacrine cells to bipolar cell terminals. Results suggest that, after a light flash, a population of glycinergic amacrine cells responds first, inhibiting a population of GABAergic amacrine cells for approximately 150 msec. The GABAergic amacrine cells feed back to bipolar terminals, only after the 150 msec delay, thus allowing the bipolar terminals to excite ganglion cells for the first 150 msec.
745	The reversal potential as well asthe complete blockade of the striatal-evokedsynaptic events by bicuculline or picrotoxin indicatethat neurotransmission between striatonigralfibers and SNr cells is due to activation of GABAAreceptors with chloride ions as charge carriers"
746	The rod-dominant ON-type bipolar cells and some bipolar cells with a small axon terminal receive negative feedback inputs from GABAergic amacrine cells
747	The role of large-conductance Ca2+-dependent K+ channels (BK) in spike broadening during repetitive firing was studied using sharp electrode and computer modelling. The amplitude of the fast after-hyperpolarization (fAHP) rapidly declined during each train. Suppression of BK-channel activity with the selective BK-channel blocker iberiotoxin, the non-peptidergic BK-channel blocker paxilline, or calcium-free medium, broadened the 1st spike to a similar degree ( approximately 60 %)
748	The Schaeffer collateral/commissural pathway elicits EPSPs in CA1 that have a large AMPA receptor-mediated component that can be blocked by CNQX
749	The Schaeffer collateral/commissural pathway elicits EPSPs in CA1 that have an NMDA-receptor mediated component that can be blocked by APV under certain experimental circumstances (such as low bath Mg+ levels). Many authors have suggested that NMDA receptors may be involved in long-term potentiation in this region. (Reviewed in
750	The subcellular distribution and biophysical properties of this current were studied in cell-attached patches. The basal dendrites were practically devoid of this conductance
751	The subcellular distribution and biophysical properties of this current were studied in cell-attached patches. Up to approximately 400um from the soma a low density of channels was found, with a 20-fold increase in the apical distal dendrite. The findings suggest that integration of synaptic input to the apical tuft and the basal dendrites occurs spatially independently due to the high Ih channel density in the apical tuft that increases the electrotonic distance between these two compartments in comparison to a passive dendrite
752	The subthalamic nucleus (STN) receives a dopaminergic innervation from the substantia nigra pars compacta.”
753	The transient voltage-gated sodium current is strong and fast in SNr GABA neurons. When a sufficient amount of the classical INaT is activated by subthreshold depolarization induced by TRPC3 channels and INa,p [persistent], the regenerative fast rising phase of the action potential is triggered ”
754	The vast majority of Nav1.1 labeling in axons was specifically localized at myelinated portions of the axon. Consistent with previous observations, Nav1.2 was found mainly in small unmyelinated axons and Nav1.6 was specifically associated with nodes of Ranvier. A low level of labeling for each type of sodium channel was also found in axon terminals.”
755	The way that different parts of a neuron carry out multiple information processing roles is illustrated by the CA1 pyramidal cell in the hippocampus. The authors used 2-photon microscopy to obtain high resolution images of calcium signals in the apical dendrites while activating Schaffer collateral inputs to induce long-term potentiation (LTP) of different durations. Short-duration LTP (LTP 1) was associated with Ca increase in dendritic spines, due to activation of NMDA receptors and local ryanodine receptors (RyRs). Intermediate duration LTP (LTP 2) was associated with Ca increase in dendritic branches, due to activation of NMDA receptors and local IP3 receptors (IP3Rs). For Ca increase in long duration LTP (LTP3), see Ca channels in CA1 pyramidal cell apical dendrite. ...
756	There is a selective localization of GABA receptors at symmetric synaptic junctions and of glutamate receptors at asymmetric junctions
757	There is also evidence that Zn+ can modulate bicuculline-sensitive responses to GABA early in development in rat (studied less than 8 days old)
758	There is no synaptic inhibition in this cell
759	These channels "prevent initiation of an action potential in the dendrites, limit the backpropagation of action potentials into the dendrites, and reduce excitatory synaptic events"
760	These channels are assembled from subunits of the Kv3 family and are necessary for the fast spiking phenotype of O/A interneurons
761	These factors all point to Kv2 family channels as being responsible for the slowly deactivating, slowly inactivating delayed rectifier in GP neurons."
762	These factors may contribute to greater susceptibility of endopiriforn nucleus to epileptogenesis. Reviewed in
763	These results suggest that serotonergic afferents from raphe dynamically modulate olfactory processing through distinct effects on multiple OB targets, and may alter the degree to which OB output is shaped by inhibition during behavior.
764	This channel is present in high density in all species. Original intracellular recordings suggesting site of impulse initiation is the axon hillock with backspread into the soma dendrites
765	This conductance triggers impulses in dendrites and soma, leading to Ca-dependant K conductances
766	This current "may be of limited significance within the normal physiological range of potential and extracellular environment"
767	This current is inactivated at rest and de-inactivated by hyperpolarization; sequences of hyperpolarization-depolarization therefore activate I A, producing the pauser reponse
768	This current is reduced by activation of the metabotropic glutamate receptors
769	This current was measured in nucleated patches from O/A interneurons and found to be ~19% of the total potassium current
770	This current was studied by combining intracellular recordings and two-photon microscopy imaging of [Ca]i
771	This current was studied using whole-cell and perforated patch-clamp in O/A interneurons
772	This is fast activating. There is also I P which is A-like but slowly activating. Some kinetic properties of this current were studied in cell-attached recordings in rats
773	This is only observed in rods in salamander.
774	This is the non-selective Na and K current located in the plasma membrane of the distal segment. It is activated in the dark by cyclic GMP from the disc membranes.
775	This is the non-selective Na and K current located in the plasma membrane of the distal segment. It is activated in the dark by cyclic GMP from the disc membranes.
776	This persistant conductance may be activated by the NMDA receptor depolarization, providing a mechanism for graded, voltage dependent EPSP amplification
777	Three types of glutamate receptors for 1) cone-activated receptors of HCs; 2) cone-activated receptors of OFF-BPs; and 3) rod-activated receptors found in HCs and BPs
778	Thus there is a steady-state calcium current contributing to the depolarization phase of the oscillation but small in comparison with the sodium current."
779	Tonically active at rest; induces a sag in hyperpolarizing responses; blocked by ACh.
780	Transients and kinetics for these channels were studied using whole-cell patch clamp recordings
781	TTX-resistant
782	TTX-sensitive
783	TTX-sensitive sodium current (possibly of the transient type?) may also be present
784	Two soluble guanylyl cyclases have been cloned and expressed
785	Two types of A-like current were observed in GP neurons: a high-threshold, TEA-sensitive current attributable to Kv3.4 channels and a low-threshold, TEA-insensitive current attributable to Kv4 family channels.”
786	Two types of PG cells can be distinguished by the presence of delayed-rectifier. R-type has DR current and shows outward rectification under current-clamp; N-type does not. A third type, X-type, has properties of both R- and N-type. Zinc modifies the A-type current, but not the delayed-rectifier type: at given voltages, it reduces A-current peak amplitude, slows its kinetics. Zinc shifts activation and inactivation toward more positive voltage. Thus, at physiological resting potential -55mV, zinc accelerates repolarization.
787	Type 1 synapse
788	Types and distribution of voltage-gated K+ channels in the soma and apical dendrites were studied in acute brain slices
789	Unlike postsynaptic NMDAR's, they are potentiatedby physiologically relevant concentrations of taurine
790	Unlike the retinogeniculate input, the corticogeniculate input is received by both ionotropic and metabotropic glutamate receptors
791	Unpublished data by Chen and Shepherd have revealed a long lasting after hyperpolarization following a train of action potentials. Using whole-cell recordings, the kinetic properties of this current have been investigated in neurones from neonatal rats, which were retrogradely labelled and identified after enzymatic dissociation
792	Using a monoclonal antibody
793	Using a whole chick (Gallus domesticus) basilar papilla preparation, a map of changes in potassium currents of tall hair cells was produced. All cells recorded from expressed IKCa and IK. The amplitude of total outward current increased in a gradient along the tonotopic axis
794	Using a whole chick (Gallus domesticus) basilar papilla preparation, it was found that apical cells expressed I-IR
795	Using Ca2+ imaging, full action potential invasion throughout the length of the basal dendrites, suggesting the presence of Na channels at somatic density, was observed by
796	Using Ca2+ imaging, full action potential invasionthroughout the length of the basal dendrites, suggesting the presence ofNa channels at somatic density, was observed by
797	Using calcium imaging, calcium waves in layer 2/3 and layer 5 neocortical somatosensory pyramidal neurons were examined in slices from 2- to 8-week-old rats
798	Using confocal microscopy, these channels were found to be localized on the soma, dendrites, and a subpopulation of dendritic spines
799	Using conventional or perforated-patch whole cell recordings, SNc neurons acutely dissociated from P4 to P16 rats NMDA (100 nM, V(hold) = -60 mV) evoked inward, APV-sensitive currents (56.4 +/- 8.6 pA) in all tested neurons (n = 29). Strong depolarizing responses were observed under current-clamp
800	Using differential polarization through applied electric fields, cell bodies and dendrites have been activated in effective isolation during intracellular recordings in vitro. In neurons located in the rostral substantia nigra, the dendrites are shown to have both HVA and LVA channels. HVA conductance appears to be exclusively dendritic. By contrast, in more caudally located cells HVA calcium spikes were located principally in the cell body
801	Using double-staining techniques, the distribution of NADPH-diaphorase (ND)- and nitric oxide synthase (NOS)-positive cells was compared in the periglomerular region of typical and atypical rat olfactory glomeruli. The number of ND/NOS-stained periglomerular cells was much higher (P &lt 0.001) in typical than in atypical glomeruli.
802	Using electrophysiological recordings and imaging, the density of these channels was found to rapidly decrease with distance from soma
803	Using electrophysiological recordings and imaging, the density of these channels was found to rapidly decrease with distance from soma and clustered in high density around the base of dendrites
804	Using ex vivo slices of guinea pig midbrain, we show that SNr GABAergic neurons express transient receptor potential melastatin 2 (TRPM2) channels that underlie NMDA-induced burst firing. Furthermore, we show that spontaneous firing rate and burst activity are modulated by the reactive oxygen species H(2)O(2) acting via TRPM2 channels. Thus, our results indicate that activation of TRPM2 channels is necessary for burst firing in SNr GABAergic neurons and their responsiveness to modulatory H(2)O(2).”
805	Using ex vivo slices of guinea pig midbrain, we show that SNr GABAergic neurons express transient receptor potential melastatin 2 (TRPM2) channels that underlie NMDA-induced burst firing. Furthermore, we show that spontaneous firing rate and burst activity are modulated by the reactive oxygen species H2O2 acting via TRPM2 channels. Thus, our results indicate that activation of TRPM2 channels is necessary for burst firing in SNr GABAergic neurons and their responsiveness to modulatory H2O2.”
806	Using in vitro methods, the modulatory actions of 5HT were examined on three different calcium-insensitive K-currents among others
807	Using intra- and extracellular recordings in ferret it has been shown that these neurons interact locally through the activation of GABA-A receptor-mediated inhibitory potentials
808	Using outside-out patches and a fast application system the properties and distribution of synaptic glutamate receptors an approximately twofold increase in AMPA-mediated current was observed in the dendritic region that receives a uniform density of Schaffer collateral input (100-250um from soma)
809	Using radioactive in situ hybridization methods, heavy labeling for NMDAR1 subunit was observed in all major CN neuronal types with lower labeling for NMDAR2A, 2B, 2C, and 2D mRNA
810	using whole-cell patch-clamp recordings from freshly dissociated mouse neocortical pyramidal neurons showed that Ca2+-dependent K+ currents were activated by Ca2+ entry through both N- and L-type channels
811	Using whole-cell recordings, the kinetic properties of this current have been investigated in neurones from neonatal rats, which were retrogradely labelled and identified after enzymatic dissociation
812	Variable densities of active channels support variable extents of backpropagating impulse in the dendrites
813	Voltage-clamp analysis suggested that IAHP in DG neurones is generated by about 1200 channels, and that about 60% are open at the peak of a maximal IAHP
814	Voltage-dependent Ca currents are seen in isolated bipolar cells
815	Voltage-gated sodium channels were found throughout the whole dendritic tree of GP neurons, and showed a significant clustering at sites of excitatory synaptic inputs.”
816	Voltage-sensitive dye signals recorded from the glomerular layer reflect activity in periglomerular cells and that Cl- efflux through non-GABAA chloride channels contributes to the postsynaptic depolarization of these cells after olfactory nerve stimulation
817	We find that small-conductance Ca2+-activated K+ (SK) channels underlie most of the mAHP in GP neurons. This mAHP conductance is a small component of the overall outward current that flows during the subthreshold part of the oscillatory cycle, the majority of which is provided instead by an inactivating K+ current."
818	Whereas, activation of the adenosine A1 receptor reduces synaptic strength by modulating presynaptic calcium channels, baclofen modulates presynaptic calcium channels as well, but also affects release processes downstream from calcium entry
819	which is important for the induction of long term changes in synaptic strength"
820	While nicotinic and muscarinic acetylcholine receptors exist in FSI-SPN synapses, only the nicotinic receptors are postsynaptic.
821	While NMDA receptor activation may be necessary for LTP at the commissural/associational synapses
822	Whole cell and perforated patch recordings in slices showed bicuculline-dependent and ?independent GABA currents from juvenile rats, suggesting two types of GABAergic inputs. The bicuculline-independent component was present only at the earliest stages of maturation, had a later peak, slower time course of decay, and marked outward rectification. A trophic or signaling role rather than primarily inhibitory was suggested for this current
823	Whole cell recording experiments have revealed a sustained, partially nimodipine-sensitve current in steps to -50mV, suggesting that they play a role in CA2+ signalling at low voltages as well as a their classical high voltages
824	Whole cell recording experiments have revealed a sustained, partially nimodipine-sensitve current in steps to -50mV, suggesting that they play a role in CA2+ signalling at low voltages as well as a their classical high voltages
825	Whole cell recording from acutely isolated rat CA3 pyramidal neurons revealed a transient (59 msec decay time constant) that was inhibited by Ni2+ and amiloride
826	Whole cell recordings from acutely dissociated neurons exhibited a R-type currents that were characterized as HVA by their rapid deactivation kinetics, half-activation and half-inactivation voltages, and sensitivity to depolarized holding potentials. In neocortical pyramidal neurons these currents inactivated at more negative potentials than in medium spiny neurons
827	Whole-cell and cell-attached patch-clamp recordings showed that ACh activates apamin-sensitive, "SK"-type potassium channels
828	Whole-cell patch-clamp recording of ICa from presynaptic boutons are comparable to that obtained from somatic recordings, but elevation of intracellular Ca is restricted to the presynaptic terminals, with no somatic or axonal changes observed
829	Whole-cell patch-clamp recordings showed that variations in the kinetics of the outward current contribute substantially to the determination of resonant frequency
830	Whole-cell patch-clamp recordings were used to identify and characterize ionic currents in isolated cells. All hair cells possessed an IKCa
831	Whole-cell patch-clamp recordings were used to identify and characterize ionic currents in isolated cells. In a small subset of cells, the IK was replaced by an IA. It is suggested that the kinetic properties of the ionic currents argue against electrical tuning
832	Whole-cell patch-clamp recordings were used to identify and characterize ionic currents in isolated cells. Most cells possessed a slowly activating IK, which is approximately 80% inactive at rest. In a small subset of cells, IK was replaced by an IA. It is suggested that the kinetic properties of the ionic currents argue against electrical tuning
833	Whole-cell patch-clamp recordings were used to identify and characterize ionic currents in isolated cells. Most cells possessed an Ih, which actively contributed to the resting potential
834	Whole-cell somatic recording during TTX application to proximal dendrites suggests the presence of a persistent Na current
835	Whole-cell voltage-clamp recordings showed that a low-threshold transient (T-type) Ca2+ current was observed in 40% of neurons
836	Whole-cell voltage-clamp recordings showed that HVA currents were present in at least 95% of neostriatal neurons, but that the majority of them appeared to belong neither to the "L-type" nor the "N-type" classification
837	With a postembedding immunogold procedure, it has been found that these receptors do not appear to be concentrated in clusters on dendrites, suggesting that the presynaptic effects of glutamate are mediated by a small complement of extrasynaptic receptors
838	With whole-cell patch clamp, two types of A-current were found in rat neostriatal neurons, one similar to previous descriptions in mammals and a second activated at considerably more depolarized potentials
839	With whole-cell recordings the properties of a voltage-dependent Na+ currents were investigated in 42 DGC acutely isolated from the resected hippocampus of 20 patients with therapy-refractory temporal lobe epilepsy (TLE) using the whole-cell patch-clamp technique.The kinetic properties contributed to a reduction of the Na+ currents during repetitive stimulation that was more pronounced with higher stimulation frequencies and also showed a dependence on the holding potential
840	Young and Oertel, in
841	Zn2+ modulates the inhibitory interaction between amacrine and bipolar cells, particularly that mediated by the GABA(C) receptor