Annika Abramson
Pronouns: she/her
Research Mentor(s): Irina Zhang
Research Mentor School/College/Department: Pharmacology / Medicine
Program: UROPF
Session: Session 7 (4:40pm – 5:30pm)
Authors: Annika Abramson
Abstract
Calcium in pancreatic beta cells are critical in triggering insulin secretion based on glucose feedback. Diabetes occurs when people can’t produce or cannot use insulin. We aimed to determine the effects of ER calcium channel activators and blockers (caffeine, CPA, dantrolene and carbachol) on cytosolic calcium in mouse pancreatic beta cells. There is currently a misunderstanding in existing literature on how cytosolic calcium is regulated in response to ER calcium release. We hypothesize that cytosolic calcium is only transiently affected in response to ER calcium release in the absence of external calcium outside of the plasma membrane. To test the hypothesis, pancreatic islets were extracted from wildtype mice. Cytosolic calcium was recorded in intact islets using fluorescence dye Fura-2am, and ER calcium was recorded using a FRET probe D4ER carried by adenovirus. The Fura-2 (340/380 nm) ratio was observed firstly in a 5 mM glucose solution, and then caffeine, CPA or carbachol was added to the solution acutely. We found that when these drugs respectively led to a sharp increase in Fura-2 Ratio and a decrease in D4ER ratio in the presence of 5 mM glucose solution. However, in the absence of external calcium, the increase of cytosolic calcium was only transient. Thus, cytosolic calcium can only be transiently regulated by ER calcium release in the absence of external calcium. Understanding how calcium is regulated in beta cells is important to promote insulin secretion in diabetes.
