Description:

Please join the Department of Pharmacology for a Works-in-Progress presentation by Andrew Shum and Bill Nobis.

Andrew Shum - DGP Student in Richard Miller and Murali Prakriya's Laboratories

"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. Moreover, 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 unclear. The goal of this study is to examine the functional relevance of chemokine signaling and CRAC channels in regulating NSC function in the brain.

Bill Nobis, M.D., Ph.D. - Adult Clinical Epilepsy Fellow/Postdoc in Geoffrey Swanson's Laboratory

"Is Synchronized Excitatory Input to Hilar Mossy Cells from CA3 Important for Epileptogenesis?"

The epileptogenic process in the hippocampus has been well studied; however, there are still many aspects of the epileptic circuit that have yet to be fully evaluated. Hilar mossy cells (HMCs) of the hippocampus figure prominently in models of epilepsy and their death has been shown to correlate with seizure frequency in both humans and animal models. It is unknown why HMCs remain so vulnerable or what role surviving mossy cells may play in circuit alteration and epilepsy. We found that HMCs receive significant excitatory input from the CA3 region that include bursts of spontaneous network activity in disinhibited conditions. Strong excitation of HMCs during synchronous CA3 activity represents a route of significant excitatory network generation back to dentate granule cells and might be important in generating epileptic networks and driving HMC death.