Journal of Neuroscience, Vol 7, 2273-2284, Copyright © 1987 by Society for Neuroscience
Dopaminergic mechanisms underlying the reduction of electrical coupling between horizontal cells of the turtle retina induced by d-amphetamine, bicuculline, and veratridine
M Piccolino, P Witkovsky and C Trimarchi
Previous studies have shown that dopamine, bicuculline, or d- amphetamine
reduce the electrical and dye-coupling between the axon terminals of the
horizontal cells of the turtle retina (see Piccolino et al., 1984). In the
present study we observed similar effects following the application of
veratridine. The actions of all these drugs were prevented by dopamine
antagonists acting on D1 receptors such as flupenthixol and SCH 23390.
However, in contrast to dopamine, the actions of d-amphetamine,
bicuculline, and veratridine were attenuated or abolished by
pharmacological agents (such as 6-OH- dopamine, alpha-methyl-p-tyrosine, or
reserpine) known to reduce the release of dopamine from dopaminergic
neurons. Moreover, the actions of veratridine and bicuculline were
prevented by tetrodotoxin, indicating that one or more neurons in the
dopamine pathway are spike-generating. We conclude that d-amphetamine,
bicuculline, and veratridine reduce electrical coupling between the axon
terminals of the turtle horizontal cells by promoting the release of
endogenous dopamine from the dopaminergic amacrine cells previously
identified (Witkovsky et al., 1984). Electron-microscopic observations
revealed that 6-OH-dopamine selectively attacked this population of
amacrine cells. No degenerating terminals were found adjacent to the
horizontal cell axon terminals. On this basis, we postulate that dopamine
reaches the horizontal cell by diffusion through the extracellular space.
