A number of putative neurotransmitter substances and their antagonists were applied to the carp retina while intracellular recordings from L-type cone horizontal cells were made. Of all the substances tested, L-aspartate was found to be the most potent agent in depolarizing these horizontal cells in dark-adapted, partially light-adapted, and Co2+-treated retinas. Furthermore, DL-a-aminoadipate, an L-aspartate antagonist, blocked the effects of both the endogenous photoreceptor transmitter and exogenously applied L-aspartate on the horizontal cells. The results suggest that L-aspartate and the natural transmitter interact with the same population of postsynaptic receptors in the horizontal cell membrane.In darkness, the vertebrate photoreceptor is partially depolarized by a sodium current that flows into the outer segment of the cell (1). This depolarization appears to result in a continuous release of neurotransmitter from the receptor onto second-order neurons (2). Light, by supressing the sodium current, hyperpolarizes the photoreceptor and depresses the release of transmitter (3, 4). The light response of second-order neurons (the horizontal and bipolar cells) is thus caused by a decrease of neurotransmitter secretion from the receptor terminal.Horizontal cells and one subclass of bipolar cell [the hyperpolarizing bipolar cell (HBC)] hyperpolarize in response to light; another subclass of bipolar cell [the depolarizing bipolar cell (DBC)] depolarizes in light. It is reasonable to assume, therefore, that, if the photoreceptor transmitter acts directly on these elements, it will depolarize horizontal cells and the HBC and hyperpolarize the DBC. Blockade of transmitter release from the receptor terminals, on the other hand, should mimic the effects of light on these cell types (5-7).