Dopamine Inhibits Forskolin‐ and 3‐Isobutyl‐1‐Methylxanthine‐Induced Dark‐Adaptive Retinomotor Movements in Isolated Teleost Retinas

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Abstract
The mechanisms of diurnal and circadian regulation of teleost retinomotor movements were investigated. In the retinas of low vertebrates, photoreceptors and melanin pigment granules of the retinal pigment epithelium (RPE) undergo movements at dawn and dusk. These movements continue to occur at subjective dawn and dusk in animals maintained in constant darkness. Cone myoids contract at dawn and elongate at dusk; RPE pigment disperses into the epithelial cells'' long apical processes at dawn and aggregates into the cell bodies at dusk. Forskolin, an adenylate cyclase activator, and 3-isobutyl-1-methylxanthine (IBMX), a phosphodiesterase inhibitor, each induces dark-adapative cone and RPE retinomotor movements in isolated light-adapted green sunfish retinas cultured in constant light. Forskolin induces a 22-fold elevation in retinal cAMP content. Forskolin- and IBMX-induced movements are inhibited .apprx. 65% and 95%, respectively, by 3,4-dihydroxyphenylethylamine (dopamine). Dopamine does not inhibit dark-adaptive movements induced by dibutyryl cAMP. Epinephrine is much less effective than dopamine in inhibiting forskolin-induced movements, while phenylephrine and clonidine are totally ineffective. Treatments that increase intracellular cAMP content promote dark-adaptive retinomotor movement. Dopamine inhibits adenylate cyclase activity in photoreceptors and RPE cells and thereby favors light-adaptive retinomotor movements.

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