Physiological and pharmacological mechanisms of glutamatergic, GABAergic and glycinergic synapses in the tiger salamander retina were studied. We used immunocytochemical and autoradiographic methods to study localizations of these
neurotransmitters and their uptake transporters; and electrophysiological methods (intracellular, extracellular and whole cell patch
electrode recordings) to study the light responses, miniature postsynaptic currents and
neurotransmitter-induced postsynaptic currents in various retinal neurons. Our results are consistent with the following scheme:
Glutamate is used by the photoreceptor and bipolar cell output synapses and the release of
glutamate is largely mediated by
calcium-dependent vesicular processes. The postsynaptic
glutamate receptors in DBCs are
L-AP4 receptors, in HBCs, HCs and
ganglion cells are the
kainate/
AMPA and
NMDA receptors. Subpopulations of HCs make GABAergic synapses on cones and gate
chloride condunctance through GABAA receptors. GABAergic HCs do not make feedforward synapses on bipolar cell dendrites and the
neurotransmitter identity of the HCs making feedforward synapses is unknown. Subpopulations of amacrine cells make GABAergic synapses on bipolar cell synaptic terminals, other amacrine cells and
ganglion cells and
GABA gates
chloride conductances in theses cells. Glycinergic amacrine cells make synapses on bipolar cell synaptic terminals, other amacrine cells and
ganglion cells and
glycine opens postsynaptic
chloride channels. Glycinergic interplexiform cells make synapses on bipolar cells in the outer retina and
glycine released from these cells open
chloride channels in bipolar cell dendrites.