When:
Monday, March 16, 2015
4:00 PM - 5:00 PM CT
Where: Ward Building, Conference Room 5-230, 303 E. Chicago Avenue, Chicago, IL 60611 map it
Audience: Faculty/Staff - Student - Public - Post Docs/Docs - Graduate Students
Contact:
Kristina Lynn Ballard
(312) 503-4892
Group: Department of Pharmacology Seminars
Category: Academic
*Tristan Hedrick, Postdoctoral Fellow
The Role of Kainate Receptors in Modulating Hilar Network Excitability
Temporal lobe epilepsy, typified by hilar network hyperexcitability, is associated with aberrant expression of kainate receptors in the dentate gyrus. Kainate receptors modulate synaptic and intrinsic excitability via ionotropic and metabotropic functions elsewhere in the hippocampus, however their role in hilar network function is unknown. We are using knockout mouse lines for various kainate receptor subunits and associated proteins to determine how changes in kainate receptor expression or function alters hilar excitability. These studies will pave the way for future studies which examine how kainate receptor function is altered in pathological conditions such as temporal lobe epilepsy.
*Andrew K. Shum, Graduate Student
Store-Operated Calcium Signaling in Neural Stem Cells
In many non-excitable cells, mobilization of Ca2+occurs through the opening of store-operated CRAC channels. Recently, we have shown the role of CRAC channels in neural stem cells (NSCs) as a pathway for Ca2+entry and its effects on NSC proliferation. Furthermore, Ca2+can play an instructive role in regulating other processes such as migration and differentiation. Chemokines are secreted regulatory factors that are important in neurogenesis and migration. However, how NSCs generate Ca2+signals in response to chemokines remains unknown. The goal of this study is to examine the functional relevance of chemokine signaling and CRAC channels in regulating NSC function in the normal and stroke-injured brain.