Format

Send to

Choose Destination
See comment in PubMed Commons below
Vis Neurosci. 1992 Sep-Oct;9(3-4):271-8.

Glutamate antagonists that block hyperpolarizing bipolar cells increase the release of dopamine from turtle retina.

Author information

1
Sensory Sciences Center, Graduate School of Biomedical Sciences, University of Texas Health Science Center, Houston 77030.

Abstract

Some neurochemical features of the neuronal circuitry regulating dopamine release were examined in the retina of the turtle, Pseudemys scripta elegans. Glutamate antagonists that block hyperpolarizing bipolar cells, such as 2,3 piperidine dicarboxylic acid (PDA), produced dose-dependent dopamine release. In contrast, the glutamate agonist 2-amino-4-phosphonobutyric acid (APB), which blocks depolarizing bipolar cell responses with high specificity, had no effect on the release of dopamine. The gamma-aminobutyric acid (GABA) antagonist, bicuculline, also produced potent dose-dependent release of dopamine. The release of dopamine produced by PDA was blocked by exogenous GABA and muscimol, suggesting that the PDA-mediated release process was polysynaptic and involved a GABAergic synapse interposed between the bipolar and dopaminergic amacrine cells. The only other agents that produced dopamine release were chloride-free media and high extracellular K+; in particular, kainic acid and glutamate itself were ineffective. These results suggest that the primary neuronal chain mediating dopamine release in the turtle retina is: cone----hyperpolarizing bipolar cell----GABAergic amacrine cell----dopaminergic amacrine cell.

PMID:
1327088
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Loading ...
    Support Center