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Connexin43 null mutation increases infarct size after stroke.

R Siushansian1, J F Bechberger, D F Cechetto

  • 1Department of Anatomy and Cell Biology, The University of Western Ontario, London, ON, Canada N6A 5C1.

The Journal of Comparative Neurology
|December 18, 2001
PubMed
Summary
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Reduced expression of connexin43 (Cx43) impaired gap junctional intercellular communication (GJIC) in astrocytes. This reduction in GJIC led to larger brain infarct volumes in Cx43 heterozygous mice following stroke, suggesting GJIC enhances neuroprotection.

Area of Science:

  • Neuroscience
  • Cellular Biology
  • Pathology

Background:

  • Glial-neuronal interactions are crucial for brain function and neuroprotection.
  • Gap junctional intercellular communication (GJIC) is a key pathway for cellular interaction.
  • Astrocytes utilize connexin43 (Cx43) for gap junctions, forming a functional syncytium for spatial buffering.

Purpose of the Study:

  • To investigate the role of Cx43-mediated GJIC in astrocytes in neuroprotection.
  • To determine the impact of reduced Cx43 expression on brain infarct volume after ischemic injury.

Main Methods:

  • Utilized heterozygous Cx43 null mice with reduced Cx43 expression.
  • Assessed Cx43 protein levels and GJIC in cultured astrocytes via Western blot.
  • Quantified brain infarct volume in wild-type and heterozygous mice after induced focal ischemia (middle cerebral artery occlusion).

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Main Results:

  • Astrocytes from heterozygote mice showed reduced Cx43 protein levels and GJIC.
  • Adult heterozygote cerebrum had 40% less Cx43 compared to wild-type.
  • Cx43 heterozygous null mice exhibited significantly larger infarct volumes (14.4 mm³) than wild-type mice (7.7 mm³) after stroke.

Conclusions:

  • Reduced Cx43 expression and impaired GJIC in astrocytes exacerbate ischemic brain injury.
  • Augmenting GJIC in astrocytes may offer a neuroprotective strategy against ischemic damage.