Google Search
CNS Seminar - Roger Thompson - Neuronal Death During Stroke

The Centre for the Neurobiology of Stress welcomes Dr. Roger Thompson from the Brain Research Centre at UBC who will present a seminar titled:

"Novel Mechanisms of Neuronal Death during Stroke"

Abstract:

Excitotoxicity is the process whereby neurons die due to dysregulation of ionic fluxes during over stimulation. During stroke, excitotoxicity in the infarct results from ischemia (O2 / glucose deprivation; OGD). Infarct expansion is thought to involve neuronal death from over activation of NMDA receptors. Both ischemia and NMDA kill neurons by necrosis and this has been associated with activation of a large cation current (Connor and Cormier (2000), J Neurophys. 83:90; Lipton (1996)). The hypothesis that ionic dysregulation and necrosis during ischemia and NMDA receptor activation is mediated by the opening of half gap junctions, or hemichannels was tested. OGD or NMDA activated a large linear current that was sensitive to carbenoxolone (Cbx) and La3+, suggesting the involvement of hemichannels. Confirmation of hemichannel activation was achieved by measuring the flux of large fluorescent dyes across the plasma membranes of acutely isolated neurons and neurons in brain slices during exposure to OGD or NMDA. These dye fluxes were sensitive to Cbx. Cell-attached patch single-channel recordings demonstrated that OGD activated Cbx-sensitive channels with a conductance of ~530 pS. This suggests that the identity of the hemichannel is pannexin 1 (Panx1), a member of newly described family of gap junction forming proteins. Thus, Panx1 hemichannel opening likely represents a major pathway for ion and metabolite dysregulation during excitotoxic stimuli that induce neuronal necrosis.

All Faculty, Staff and Students are welcome

Light refreshments served




© University of Toronto Scarborough