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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