Sodium action potentials are not required for light-evoked release of GABA or glycine from retinal amacrine cells.
Although most CNS neurons require sodium action potentials (Na-APs) for normal stimulus-evoked release of classical neurotransmitters, many types of retinal and other sensory neurons instead use only graded potentials for neurotransmitter release. The physiological properties and information processing capacity of Na-AP-producing neurons appear significantly different from those of graded potential neurons. To classify amacrine cells in this dichotomy, we investigated whether Na-APs, which are often observed in these cells, are required for functional light-evoked release of inhibitory neurotransmitters from these cells. We recorded light-evoked inhibitory postsynaptic currents (IPSCs) from retinal ganglion cells, neurons directly postsynaptic to amacrine cells, and applied TTX to block Na-APs. In control solution, TTX application always led to partial suppression of the light-evoked IPSC. To isolate release from glycinergic amacrine cells, we used either bicuculline, a GABAA receptor antagonist, or picrotoxin, a GABAA and GABAC receptor antagonist. TTX application only partially suppressed the glycinergic IPSC. To isolate release from GABAergic amacrine cells, we used the glycine receptor blocker strychnine. TTX application only partially suppressed the light-evoked GABAergic IPSC. Glycinergic and GABAergic amacrine cells did not obviously differ in the usage of Na-APs for release. These observations, in conjunction with previous studies of other retinal neurons, indicate that amacrine cells, taken as a class, are the only type of retinal neuron that uses both Na-AP-dependent and -independent modes for light-evoked release of neurotransmitters. These results also provide evidence for another parallel between the properties of retinal amacrine cells and olfactory bulb granule cells.
Bieda
M C
MC
Departments of Ophthalmology and Physiology, UCSF School of Medicine, San Francisco 94143, California.
Copenhagen
D R
DR
D000200:Action Potentials / Q000502:physiology; D000557:Ambystoma; D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D005998:Glycine / Q000378:metabolism*; D018684:Glycine Agents / Q000494:pharmacology; D066298:In Vitro Techniques; D010775:Photic Stimulation; D010852:Picrotoxin / Q000494:pharmacology; D012160:Retina / Q000166:cytology / Q000378:metabolism*; D026941:Sodium Channel Blockers; D015222:Sodium Channels / Q000502:physiology*; D013331:Strychnine / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D001640:Bicuculline; D018756:GABA Antagonists; D005998:Glycine; D018684:Glycine Agents; D010852:Picrotoxin; D026941:Sodium Channel Blockers; D015222:Sodium Channels; D013331:Strychnine; D013779:Tetrodotoxin; D005680:gamma-Aminobutyric Acid