Neurotransmitter inputs to directionally sensitive turtle retinal ganglion cells.
Synaptic drugs were superfused into turtle eyecup preparation while recording extracellularly from directionally sensitive (DS) retinal ganglion cells. As in previous experiments in intact rabbit retina, both picrotoxin (a GABA antagonist) and physostigmine [an acetylcholine (ACh) potentiator] reduced or eliminated the directional selectivity of these cells. These drug effects occurred at micromolar concentrations and were long lasting. Superfusion of ACh caused excitation, and GABA caused inhibition of the spike activity of these DS cells. In some experiments, the ganglion cell was isolated from its presynaptic inputs by perfusing with a low-Ca2+/EGTA perfusate, which blocked synaptic transmission but did not suppress spike firing. During this synaptic block, ACh still caused spontaneous spike firing, and GABA was able to suppress the ACh-induced spike activity. Strychnine slightly increased the spontaneous activity of DS ganglion cells and reduced their response to light. Glycine and taurine were equally effective in totally suppressing spike activity, and strychnine blocked this inhibition by both agents. However, these inhibitory effects may be transynaptic because glycine did not suppress ACh-induced excitation during synaptic block. Superfusion of micromolar concentrations of methionine enkephalin and [D-Ala2]methionine enkephalinamide occasionally caused small increases in the light responses of DS cells, whereas naloxone, a broad-spectrum opiate antagonist, moderately decreased light responsiveness. Because naloxone had no effect on these cell's directional tuning, the opiate system is probably not involved in the mechanism of directional sensitivity. Based on the effects of these transmitter candidates and their antagonists, a possible site fo DS subunits may be the ACh and GABA receptors on the membrane of DS ganglion cells. ACh provides light-evoked excitation that may, when potentiated by physostigmine, overcome asymmetric GABA inhibition. Although the role of glycine in directional sensitivity is small, it may be responsible for regulating presynaptic excitatory pathways leading to the DS ganglion cells.
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D000818:Animals; D002799:Cholinergic Fibers / Q000502:physiology; D004744:Enkephalin, Methionine / Q000494:pharmacology; D005998:Glycine / Q000502:physiology; D009039:Motion Perception / Q000502:physiology*; D009270:Naloxone / Q000494:pharmacology; D018377:Neurotransmitter Agents / Q000502:physiology*; D012160:Retina / Q000502:physiology*; D012165:Retinal Ganglion Cells / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects; D013654:Taurine / Q000502:physiology; D014426:Turtles / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D018377:Neurotransmitter Agents; D013654:Taurine; D009270:Naloxone; D005680:gamma-Aminobutyric Acid; D004744:Enkephalin, Methionine; D005998:Glycine