UCLA

Circadian rhythms are endogenously-generated rhythmic bodily processes that occur with a period of approximately 24 hours. They occur at every level of biological organization, and fundamentally underlie almost every physiological, neurological, and behavioral function undergone by an organism. It should not be surprising, therefore, that circadian disturbances are a common symptom of diseases and disorders of the nervous system, and that this disturbance feeds back into the disease mechanisms to worsen symptoms. Circadian phenotypes of mouse models of Rett syndrome, Autism Spectrum Disorder, and Huntington’s disease have been extensively studied in our lab. This thesis further examines these models to determine if a common underlying histopathology is present in the suprachiasmatic nucleus (SCN), the central clock of the mammalian brain. Tracing of Nissl stains was used to determine if there were any changes in the gross morphology of the SCN, and immunohistochemistry and immunofluorescence were used to look for possible loss of SCN neuropeptide-expressing subpopulations of neurons. Ultimately, no common histoanatomical phenotype was observed between the three mouse models, leading to the conclusion that separate underlying phenotypes must be converging on common patient symptoms.