Retinal rhythms in photoreceptors and dopamine synthetic rate: and the effect of a monoamineoxidase inhibitor.

Autophagic degradation (AV) in rod inner segments undergoes a circadian rhythm that is dependent on light stimulation, being abolished in constant darkness, but persisting with dampened amplitude in constant light and reentrained after phase-shifts of the light--dark cycle. AV activity can be stimulated by light in vivo and in vitro. The monoamineoxidase type A inhibitor drug clorgyline phase delays the circadian rest-activity cycle. Clorgyline did not phase delay the rhythms of AV nor of disk-shedding, but significantly reduced AV rhythm amplitude. A rhythm of retinal dopamine (DA) level and synthetic rate persists in constant darkness, thus demonstrating the circadian nature of this rhythm. The existence of an endogenous rhythm of a putative retinal neurotransmitter may indicate some basic regulatory function of the DA system. Moreover, DA level and synthetic rate were significantly increased by clorgyline. Thus, the drug-induced reduction of retinal morphological parameters to light stimulation is paralleled by an increase of retinal DA levels. A functional relationship between the retinal DA system and photoreceptor metabolism remains to be established.