Abstract
The effects on spike discharges of acetylcholine chloride (ACh), applied electrophoretically at the inner plexiform layer, were examined in air-exposed and superfused preparations of the isolated carp retina. Most of spike-generating units examined (147 of 204 units; 72%) were sensitive to electrophoretically applied ACh. Among the ACh-sensitive ones, 125 units (85%), including all ON-center, most ON-OFF and two-thirds of OFF-center units, were activated, whereas 22 units (15%), including mainly OFF-center units, were suppressed by the agent. In retinas superfused with a medium containing 20m MMg 2+and0.5mMCa 2+, units ceased in their spontaneous and light-induced discharges, but they were activated by electrophoretically applied ACh. The ACh-induced activation was reduced in magnitude or abolished during an exposure of the retina to a medium containing hexamethonium chloride (25 μM), whereas the ACh-induced suppression was reduced by atropine sulfate (25 μM) more effectively than by hexamethonium. Therefore, the results suggest that nicotinic receptors are involved in the ACh-activation, whereas both, but predominantly muscarinic, receptors may participate in the ACh-suppression of spike discharges in the carp retina.
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