Date of Award

Fall 2022

Document Type


Degree Name

Doctor of Philosophy (PhD)


Biological Sciences

First Advisor

Evans, Jennifer A.

Second Advisor

Gilmartin, Marieke

Third Advisor

Gasser, Paul


Daily and seasonal rhythms are programmed by neural circuits that use daily timing and duration of light to anticipate predictable environmental changes (i.e., day length, temperature, food, predation). Daily and annual changes in light modulate human health to produce both positive and negative effects, but neural mechanisms underlying light-driven changes in the brain remain poorly understood. In mammals, light is processed and encoded by the brain’s central clock, the suprachiasmatic nucleus (SCN). The SCN also encodes day length (i.e., photoperiod) to regulate annual fluctuations in mammalian physiology, but it’s not clear precisely how the SCN network achieves this. One signal that may contribute to SCN photoperiod encoding is the neuropeptide somatostatin (SST). In rodents, SST expression is modulated by photoperiod in hypothalamic regions regulated by the SCN, suggesting involvement of the central clock. The SCN expresses SST but its role in central clock function and photoperiodic encoding has not been examined. Here, using a range of genetic and imaging approaches, I demonstrate that SST signaling increases circadian robustness in a sexually dimorphic manner. First, I use cellular fate-mapping approaches to demonstrate that SCN SST is regulated by photoperiod in a manner that suggests de novo Sst transcription. Next, I use a battery of circadian behavioral assays to demonstrate that SST contributes to photoperiodic entrainment and circadian responses to light in a manner influenced by sex. However, lack of SST does not alter basic circadian properties, suggesting that SST signaling modulates specific circadian characteristics under particular conditions. Third, I demonstrate that SST regulates SCN neurochemistry via influence on neurons that mediate photic responses. Further, those same cells express a subtype of SST receptor capable of resetting molecular clock function. Last, I demonstrate that lack of SST enhances SCN photoperiodic encoding by modulating photic processing and network communication in a sex-dependent manner. Collectively, these results provide new insight into mechanisms that regulate seasonality and circadian clock function in mammals. The discovery of sexually divergent clock circuits may provide new insights relevant for understanding gender disparities in seasonal/circadian disease states.

Included in

Biology Commons