Using a New Conditional Knock-out Mouse Model to Investigate Novel Calcium Signaling Pathways in the Brain
Aikaterini Britzolaki, Ben Klocke
Attention-deficit hyperactivity disorder (ADHD) affects over 8% of individuals in the US, according to the NIH. In addition to impaired attention and locomotor hyperactivity, symptoms often include enhanced impulsivity and memory deficits. The etiology of ADHD is elusive, but one proposed mechanism behind this and many other brain disorders is the dysregulation of intracellular calcium (Ca2+) homeostasis. Ca2+ is a critical second messenger for a constellation of cellular processes, including cell proliferation and death, metabolism, and gene expression. Naturally, neuronal Ca2+ signaling is vital in processes such as long-term potentiation (LTP) and synaptic transmission, among others. Interestingly, our lab has identified a new calcium-handling regulator to be expressed in the mouse brain, and that global genetic ablation of this gene in mice results in the manifestation of an ADHD-like behavioral phenotype. Our lab has recently generated a novel conditional knockout (cKO) mouse model of this gene, that also exhibits locomotor hyperactivity, a cardinal ADHD-like behavior. Further, we have employed the 5-choice serial reaction time task (5-CSRTT), a state-of-the-art behavioral paradigm to assess attentional capacity and impulsivity, two other core symptoms of ADHD. Interestingly, preliminary data from our lab show that the cKO mice exhibit impaired attention in this paradigm. Altogether, these findings strongly support a novel role for this gene in the manifestation of ADHD-like behaviors.
Primary Advisor's Department
Stander Symposium project, College of Arts and Sciences
United Nations Sustainable Development Goals
Good Health and Well-Being
"Using a New Conditional Knock-out Mouse Model to Investigate Novel Calcium Signaling Pathways in the Brain" (2022). Stander Symposium Projects. 2408.