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Post-Stroke Ischemia Opens Hemichannels in Neurons

Researchers discover gap junction hemichannels that respond to ischemia and lead to neuron death

FRIDAY, May 12 (HealthDay News) -- Researchers have discovered hemichannels in neurons that open in response to ischemia and may contribute to anoxic depolarization and neuronal cell death after stroke, according to a report in the May 12 issue of Science.

Brian A. MacVicar, Ph.D., and colleagues from the University of British Columbia in Vancouver, Canada, sought to identify the large-conductance channels responsible for neuronal excitotoxicity after stroke. A localized decrease in oxygen and glucose opens the channels, which triggers an ion flux that leads to neuronal swelling and necrosis within minutes of an infarct.

Using isolated mouse neurons and brain slices, the authors simulated ischemia-like conditions by depriving cells of oxygen and glucose. Within 10 minutes, a large conductance channel opened that was distinct from other ion channels, and could be blocked by a specific inhibitor of gap junctions/hemichannels. After opening, dyes impermeable under normal conditions could freely cross the neuronal membrane.

"Hemichannel opening contributes to the profound ionic dysregulation during stroke and may be a ubiquitous component of ischemic neuronal death," the authors write. "Hemichannel opening may be an important new pharmacological target to prevent neuronal death in stroke."

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