Elevation of cyclic AMP activates an actin-dependent contraction in teleost retinal rods.

Abstract

Agents which elevate cAMP cause teleost [Sarotherodon mossambicus] retinal rods to contract. This cAMP effect was characterized and the role of the cytoskeleton in cyclic nucleotide-induced contraction was evaluated using actin and microtubule inhibitors. The necklike myoid region of the rod contracts in the dark and elongates in the light. If long, light-adapted rods are cultured with cAMP analogs and IBMX [isobutyl methylxanthine] rods contract to their short dark-adapted position. Cyclic nucleotide-induced rod contraction occurs in constant light, requires a phosphodiesterase inhibitor, and is specific to cAMP (db [dibutyryl] cGMP, 8-bromo-cGMP, 5''AMP, and adenosine have no effect on rod myoid length). cAMP effects on rod length are consistent with observations from several species that cAMP levels are higher in dark-adapted than in light-adapted retinas. Since rod myoids contain paraxially aligned actin filaments and microtubules, we have used the motility inhibitors cytochalasin D and cold and nocodazole to investigate the roles of these cytoskeletal elements in rod contraction. Cyclic nucleotide-induced contraction is not inhibited when myoid microtubules are disrupted with cold and nocodazole treatments, but contraction is blocked if myoid actin filaments are disrupted with cytochalasin D. Evidently, actin filaments, but not microtubules, are required for rod contraction. Probably, rod contraction in vivo is triggered by a rise of cytoplasmic cAMP at onset of darkness and this contraction is mediated by an actin-dependent mechanism.