Using a Genetic Mouse Model to Investigate the Role of Calcium Signaling in Mouse Behavior
Aikaterini Britzolaki, Ben Klocke
Ca2+ is a critical second messenger for a constellation of cellular processes, and neuronal Ca2+ signaling is no exception. Indeed, disruption of neuronal Ca2+ homeostasis has been implicated in a variety of neuropsychiatric disorders. Our lab has recently identified a potential new player in the neuronal Ca2+ toolkit that is expressed in the brain. Strikingly, mice that do not express this gene (KO) present a hyperactive phenotype as compared to their wild-type (WT) counterparts. However, the underlying neurobiological mechanisms by which this phenotype manifests itself are unknown. Thus, in the context of the current project, we employed high-performance liquid chromatography (HPLC) and state-of-the-art electroencephalography (EEG) techniques to investigate the neurochemical systems and cortical rhythms that are affected by constitutive loss of this gene in mice. Indeed, our results show that KO mice exhibit neurochemical noradrenergic alterations in key brain regions associated with the pathophysiology of many neuropsychiatric disorders. Further, these mice show alterations in cortical rhythms during sleep. Overall, these data support a mechanistic role for this protein in regulating mouse behavior.
Primary Advisor's Department
Stander Symposium project, College of Arts and Sciences
United Nations Sustainable Development Goals
Good Health and Well-Being
"Using a Genetic Mouse Model to Investigate the Role of Calcium Signaling in Mouse Behavior" (2020). Stander Symposium Projects. 1879.