Investigating the Neurobiological Effects of a Novel Calcium-Handling Protein in ADHD
Aikaterini Britzolaki, Pothitos Pitychoutis, Joey Edward Saurine
Attention-deficit/hyperactivity disorder (ADHD) is an extremely prevalent and debilitating neurodevelopmental disorder that affects people of all ages. ADHD symptoms include persistent inattention, impulsivity and/or hyperactivity, accompanied by significant learning and memory deficits. Abnormal function of calcium-handling machinery has been implicated in the pathophysiology of ADHD in humans and in animal models. Intracellular calcium homeostasis in the brain is critical for cell function and survival. In the nervous system, impaired calcium homeostasis may lead to hyperactivity and learning and memory deficits, key symptoms of ADHD. Exciting preliminary data from our group support that a protein, which plays a major role in regulation of calcium homeostasis in the heart, is also expressed in a specific region of the brain that is implicated in the neurobiology of ADHD. Moreover, we have found that its genetic ablation in mice (i.e., knockout, KO) results in the manifestation of a hyperactive ADHD-relevant behavioral phenotype. In the present study, WT and KO mice were pharmacologically challenged with amphetamine and atomoxetine, two first-line drugs used for the treatment of ADHD in humans, to assess whether they rescue the ADHD-like phenotype caused by ablation of this gene. Additionally, a preliminary neurochemical analysis of striatal and prefrontocortical tissue punches by high-performance liquid chromatography (HPLC) was performed to determine baseline dopamine levels in KO and WT mice. Overall, the results of the proposed studies have shed light on the complex functions of this novel calcium-handling player in the brain suggesting it is involved in the regulation of locomotor behavior.
Primary Advisor's Department
Stander Symposium project
"Investigating the Neurobiological Effects of a Novel Calcium-Handling Protein in ADHD" (2019). Stander Symposium Projects. 1669.