Published online by Cambridge University Press: 02 June 2009
In the turtle retina, dopamine has been observed in a small population of amacrine cells. Whereas the effect of dopamine has been intensively studied, knowledge about the release of this transmitter and the neuronal control of its release are still poorly understood. We therefore decided to study the release of endogenous dopamine. Isolated retinas were superfused with Ringer’s solutions and stimulated with increased potassium, light, or drugs which interfere with neurotransmitter systems. Dopamine was analyzed by using aluminum-oxide extraction and high-pressure liquid chromatography (HPLC) with electrochemical detection. Increased potassium (25 mM) caused a five-fold increase in the basal release. When calcium was replaced by cobalt, no increase was induced by 25 mM potassium. Flickering light increased the basal release of endogenous dopamine by a factor of three. The effect of flickering light was greater in the presence of additional steady background illumination. Kainate (10 μM), an agonist for excitatory amino acids, doubled the basal dopamine release. Bicuculline (10 μM), a γ-amino butyric acid (GABA) antagonist, increased the release to about six times the basal level. Naloxone (10 μM), an opiate antagonist, increased the release to eight times the basal level. These findings suggest that dopamine is released from amacrine cells in the turtle retina in a calcium-dependent manner, which is most likely a vesicular release. Dopamine release is induced by flickering light vs. darkness and vs. steady background illumination. A moderate background illumination alone does not significantly increase basal dopamine release. Drug treatment during the release experiments suggests that dopaminergic neurons receive an excitatory input either directly or indirectly from glutamatergic bipolar and/or amacrine cells and inhibitory inputs either directly or indirectly from GABAergic amacrine cells and from enkephalinergic amacrine cells or efferent fibers.
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