Modulation of photosensitivity by serotonin in the Aplysia eye
The isolated eye of Aplysia contains a circadian pacemaker whose phase can be shifted by serotonin treatments. Clues for the localization of the pacemaker in the eye may be gained by determining which cells in the eye are sensitive to serotonin. The sensitivity of photoreceptor cells to serotonin was examined by investigating the effect of serotonin on the amplitude of the electroretinogram (ERG) from the eye. Low concentrations of serotonin produced large and long-lasting increases in the ERG. This effect of serotonin is specific because other putative transmitters (e.g., acetylcholine, octopamine, and dopamine ) do not mimic the effects of serotonin on the ERG. Serotonin also increases the frequency of optic nerve impulses from eyes exposed to constant light. These results show that the photosensitivity of the eye is increased by serotonin. Brief electrical stimulation of the optic nerve also increased the ERG for a long period of time. This suggests that efferent optic nerve activity modulates photosensitivity through release of serotonin in the eye. The mechanism by which serotonin regulates photosensitivity appears to involve an increase in intracellular cyclic AMP. An analogue of cyclic AMP, 8-benzylthio-cyclic AMP, and a phosphodiesterase inhibitor, 3-isobutyl-l-methylxanthine, each individually mimics the effect of serotonin on the ERG. Forskolin, a specific activator of adenylate cyclase, also increased the ERG. Finally, the effects of forskolin and serotonin on the ERG are nonadditive. The similar effects of serotonin and cyclic AMP on both the circadian rhythm and photosensitivity are consistent with the hypothesis that serotonin shifts the phase of the circadian rhythm by acting on photoreceptor cells in the eye.