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

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