On the Role of SERCA-dependent Calcium Handling in the Mouse Stress Response

On the Role of SERCA-dependent Calcium Handling in the Mouse Stress Response

    Presenter(s)

    Summer Annalee Istenes, Daniel F. Jevnikar, Ben Klocke, Marc Nya, Hayden Nathaniel Ott, Morgan Elizabeth Roach

    Comments

    Presentation: 9:00-10:15, Kennedy Union Ballroom

    Description

    Calcium (Ca2+), a critical second messenger, has been implicated in various cellular processes including gene transcription, muscle contraction, cell-cell adhesion, and neurotransmitter release. Previous research has implicated abnormal calcium homeostasis as contributing to attention/deficit hyperactivity disorder (ADHD), a common neurodevelopmental disorder characterized by inattention and other symptoms such as hyperactivity and impulsivity. A major regulator of cytosolic calcium concentration is the sarco-endoplasmic reticulum Ca2+ ATPase 2 (SERCA2), a protein found in the heart and brain that sequesters Ca2+ into the endoplasmic reticulum. Using a mouse model, our lab has previously found that constitutive deletion of PLN, a protein inhibitor of SERCA2, results in an ADHD-like phenotype characterized by hyperactivity, anxiolytic behavior, and cognitive deficits. In this study, we sought to understand the role of PLN in regulating stress response by assessing the effects of chronic-restraint stress in conjunction with constitutive PLN deletion on mouse behavior. The results of this study help to further our understanding of the role of PLN, SERCA2, and Ca2+ in the regulation of the brain and behavior.

    Publication Date

    4-17-2024

    Project Designation

    Independent Research

    Primary Advisor

    Pothitos Pitychoutis

    Primary Advisor's Department

    Biology

    Keywords

    Stander Symposium, College of Arts and Sciences

    Institutional Learning Goals

    Scholarship; Practical Wisdom; Vocation

    On the Role of SERCA-dependent Calcium Handling in the Mouse Stress Response

    Share

    COinS