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Ischemic Stroke ll: Pathophysiology

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An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...

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A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.Mechanisms of Transient Cerebral IschemiaTransient cerebral ischemia may arise through several mechanisms. One...

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Related Experiment Video

Updated: Jun 25, 2026

Stereological and Flow Cytometry Characterization of Leukocyte Subpopulations in Models of Transient or Permanent Cerebral Ischemia

Stereological and Flow Cytometry Characterization of Leukocyte Subpopulations in Models of Transient or Permanent Cerebral Ischemia

Published on: December 28, 2014

Hemichannels in cerebral ischemia.

Panagiotis Bargiotas¹, Hannah Monyer, Markus Schwaninger

¹Institute of Pharmacology, University of Heidelberg, Germany.

Current Molecular Medicine

|March 12, 2009

Summary

This summary is machine-generated.

Unpaired hemichannels, initially thought to be functional only in gap junctions, actively contribute to cell death during ischemia. These channels disrupt membrane permeability, leading to ionic imbalance and metabolite loss, impacting ischemic outcomes.

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Area of Science:

Cell Biology
Neuroscience
Biochemistry

Background:

Hemichannels are transmembrane channel subunits of gap junctions, typically formed by connexin or pannexin proteins.
While gap junction communication is known to mediate signal transport during ischemia, the role of unpaired hemichannels is increasingly recognized.

Purpose of the Study:

To review the properties and functions of unpaired connexin and pannexin hemichannels.
To explore the implications of unpaired hemichannel activity in pathophysiological conditions, particularly during ischemia.

Main Methods:

Literature review of studies investigating hemichannel function.
Analysis of research on the role of hemichannels in cellular processes during ischemia.

Main Results:

Unpaired hemichannels exhibit diverse activities modulated by pathophysiological conditions like ischemia.
Open hemichannels in ischemia significantly alter membrane permeability, causing cell death via ionic dysregulation, metabolite loss, and altered ATP levels.

Conclusions:

Unpaired hemichannels play a critical role in ischemia-induced cell death.
Understanding hemichannel function is crucial for comprehending events like glutamate release, oxidative stress, and cortical spreading depression during ischemic insults.