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Dopamine D 4 receptor‐mediated regulation of rod opsin mRNA expression in tiger salamander
Author(s) -
Alfinito Peter D.,
TownesAnderson Ellen
Publication year - 2001
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2001.00109.x
Subject(s) - opsin , quinpirole , dopamine , rhodopsin , biology , dopamine receptor , dopaminergic , dopamine receptor d3 , gene expression , messenger rna , agonist , endocrinology , microbiology and biotechnology , dopamine receptor d2 , medicine , receptor , biochemistry , retinal , gene
Light stimulates dopamine release in the retina and has been shown to rapidly up‐regulate rod opsin mRNA. In the present study, we tested the effect of dopamine on rod opsin mRNA expression and examined the hypothesis that dopamine can mediate a light‐evoked increase in opsin gene expression. Northern blots showed that a 30‐min light‐exposure increased rod opsin mRNA expression 27%. In situ hybridization on isolated rods showed that 500 n m dopamine and 1 µ m quinpirole (dopamine D 2 /D 3 /D 4 agonist) increased opsin mRNA 45% and 26%, respectively. The effect of quinpirole was selectively blocked by the D 4 antagonist, L750,667 (20 µ m ). In very low density cultures, quinpirole increased opsin expression 46%, suggesting a direct effect on rod photoreceptors. Consistent with a dopamine D 4 receptor mechanism, 1 µ m H‐89 (protein kinase A inhibitor) increased opsin mRNA 39%. Finally, intravitreal injection of quinpirole increased opsin mRNA 21% whereas injection of L750,667 (10 µ m ) blocked the light‐evoked increase in opsin expression. These data show that rod opsin mRNA is up‐regulated by dopamine binding a D 4 ‐like receptor on rods, possibly through inhibition of protein kinase A, and that endogenous dopamine can mediate the light‐evoked increase in opsin mRNA expression.