Name
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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