Abstract

Two general research questions were investigated in the present thesis. First, are there cellular changes in protein expression that are uniquely associated with photic entrainment? Second, which subset of retinal afferents is necessary for the transmission of photic information to the SCN? The experiments aimed at answering the first question revealed a unique pattern of Fos protein immunoreactivity in the SCN shell in response to entraining light. Specifically, light suppressed Fos protein expression in the shell region whilst inducing it in the core of rats receiving light at dawn or dusk. This complex pattern of Fos expression was also present in animals treated neonatally with monosodium glutamate (MSG), an animal model of retinal degeneration that spares photic entrainment. Further, the expression of the protein product of the clock gene Per2 was found to be rhythmic within the SCN core and shell and unaffected by entraining light. Finally, behavioral arrhythmicity produced by constant bright light exposure was found to be associated with a complete disruption of the cellular rhythm of Per2 and Fos expression in the SCN. The experiments attempting to provide answers to the second question revealed that the retinal projection to the SCN is heterogeneous and that none of the retinal fiber phenotypes examined (fibers bearing the p75 neurotrophin receptor or melanopsin) is necessary to mediate photic entrainment. In conclusion, photic entrainment is a unique event characterized by cellular changes in protein expression that differ from those induced by discrete light-induced phase shifts. Further, retinal ganglion cells of all the different phenotypes appear to contribute to the transmission of the photic input to the circadian clock in a generally redundant manner.