Abstract

Alterations to the circadian molecular clock that drive these rhythms are associated with the development of neurodegenerative diseases such as Alzheimer and Parkinson’s disease and plays a key role in neuroplasticity (Cronin et al., 2017 & Perez-Cruz et al., 2009). Among the many genes involved in regulating circadian rhythms, Bmal1 is vital for both the generation and maintenance of molecular circadian rhythms. Alterations to Bmal1 functioning are associated with severe health concerns, such as motor impairments, metabolic syndrome, and a reduction in lifespan (Tonelli et al., 2009). The circadian system consists of a master pacemaker located in the Suprachiasmatic nucleus (SCN) of the hypothalamus, and peripheral clocks that synchronize to the master clock. Among these peripheral clocks is the striatum, a major site of synaptic plasticity, and a key player in motor control, and affective behaviors. Studies in our laboratory have confirmed that Bmal1 is expressed in most neurons throughout the striatum (Frederick et
al., 2017). Currently, our understanding of local circadian regulation on neuronal plasticity in the striatum is limited. By Golgi-staining striatal sections of Bmal1 KO animals, we aim to understand the impact of deleting this crucial circadian gene on dendritic spine morphology. By utilizing the rotarod test, we also want to investigate the role of this gene in motor coordination. Results indicate that Bmal1 deletion in the principal medium spiny neurons of the striatum has an impact on motor coordination and spine branching by reducing the density of spines and their junctions. However, no such differences were found between WT and HET animals, suggesting that Bmal1 is haplo-sufficient in its role in striatal spine morphology. These results are the first to establish a role of Bmal1 in striatal dendritic morphology and could have implications for future studies on striatal connectivity.