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J H Boatright
Publications and source records attributed to J H Boatright.
Inhibition of endogenous dopamine release in amphibian retina by L-2-amino-4-phosphonobutyric acid (L-AP4) and trans-2-aminocyclopentane-1,3-dicarboxylate (ACPD).
The metabotropic glutamate receptor agonists 2-amino-4-phosphonobutyric acid (AP4) and trans-2-aminocyclopentane-1,3-dicarboxylate (ACPD) blocked light-stimulated dopamine release from Xenopus laevis retina. ACPD suppressed release in darkness but AP4 did not. AP4 blocked release stimulated in darkness by picrotoxin, a GABA-A receptor antagonist. The data suggest that regulation of dopamine release in Xenopus retina involves subpopulations of metabotropic glutamate receptors.
Aminobutyrates↗
Stimulation of endogenous dopamine release and metabolism in amphibian retina by light- and K+-evoked depolarization.
The release and metabolism of dopamine (DA) in retina was assessed using an in vitro eye cup preparation of the African clawed frog. The concentration of DA in the incubation medium and of 3,4-dihydroxyphenylacetic acid (DOPAC) and DA in retinas was measured by high-performance liquid chromatography with electrochemical detection (HPLC-ED). K+-induced depolarization stimulated DA overflow from the eye cups into the incubation medium and increased tissue DOPAC levels in dark-adapted retinas. Basal and K+-stimulated DA overflow and DOPAC accumulation were Ca2+-dependent. Exposure of dark-adapted retinas to constant white light for 1 h also increased DA overflow and DOPAC levels, while 1 h of alternating 10 s periods of light and dark had no effect. The results indicate that DA release and metabolism may be stimulated as a function of light-adaptation.
3,4-Dihydroxyphenylacetic Acid↗
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.
1-Methyl-3-isobutylxanthine↗