Stroke, Ischemia, and Ion Flux

Science's STKE  16 May 2006:
Vol. 2006, Issue 335, pp. tw167
DOI: 10.1126/stke.3352006tw167

The rapid decrease of oxygen and glucose in brain tissue after an acute stroke can trigger necrotic neuronal cell death within minutes. The main underlying cause is the dysregulation of major intracellular ion concentrations, but it has been unclear which particular ion channels are activated by ischemic conditions in pyramidal neurons. Pannexin 1 (Px1) is a member of a family of gap junction proteins that are highly expressed in pyramidal neurons. In acutely isolated neurons and brain slices, Thompson et al. found that Px1 hemichannel opening was activated by ischemic stress. Thus, hemichannel activation by ischemia during stroke could be responsible for the profound ionic dysregulation contributing to excitotoxicity.

R. J. Thompson, N. Zhou, B. A. MacVicar, Ischemia opens neuronal gap junction hemichannels. Science 312, 924-927 (2006). [Abstract] [Full Text]