Dopamine mediates the light-evoked suppression of serotonin N-acetyltransferase activity in retina.
The possible role of dopamine in the light-induced suppression of serotonin N-acetyltransferase (NAT) activity in retinas of the African clawed frog (Xenopus laevis) was investigated using an in vitro eye cup preparation. The nocturnal increase of retinal NAT activity was significantly inhibited by either light exposure or exogenous dopamine. Spiperone, a dopamine receptor blocker, antagonized this inhibitory effect of light on NAT activity, but had no effect in darkness. The effect of spiperone required the presence of cyclic nucleotide phosphodiesterase inhibitors, 3-isobutylmethylxanthine (IBMX), papaverine, or Ro 20-1724. Under the conditions employed in this study, neither spiperone nor the phosphodiesterase inhibitors significantly affected NAT activity when added alone. This observation suggests a synergistic interaction between the dopaminergic antagonists and the phosphodiesterase inhibitors. Other dopamine receptor blockers, including haloperidol, cis-flupenthixol, clozapine and metoclopramide, increased NAT activity of light-exposed retinas incubated in the presence of IBMX. SCH 23390, a D1-selective dopamine receptor antagonist, did not increase NAT activity, nor did the alpha- and beta-adrenergic receptor antagonists tested. The effect of spiperone and IBMX on NAT activity was blocked by apomorphine and by the D2-dopamine receptor agonist LY 171555, but not by the D1-receptor agonist SKF 38393-A. The concentration of 3,4-dihydroxyphenylacetic acid was higher in light-exposed retinas than in dark-adapted retinas, suggesting that light exposure increases dopamine metabolism in Xenopus retina. The results presented in this paper suggest that dopamine, released in response to light exposure and acting on D2-dopamine receptors, is partially responsible for the light-induced suppression of the nocturnal increase in retinal NAT activity.
D015056:1-Methyl-3-isobutylxanthine / Q000494:pharmacology; D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000123:Acetyltransferases / Q000378:metabolism*; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001191:Arylamine N-Acetyltransferase / Q000378:metabolism*; D004298:Dopamine / Q000502:physiology*; D066298:In Vitro Techniques; D008027:Light; D010726:Phosphodiesterase Inhibitors; D012160:Retina / Q000201:enzymology*; D013134:Spiperone / Q000494:pharmacology; D014982:Xenopus laevis
D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D010726:Phosphodiesterase Inhibitors; D015102:3,4-Dihydroxyphenylacetic Acid; D013134:Spiperone; D000123:Acetyltransferases; D001191:Arylamine N-Acetyltransferase; D015056:1-Methyl-3-isobutylxanthine; D004298:Dopamine