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Related Experiment Videos

Increase in synaptophysin immunoreactivity following cortical infarction.

R P Stroemer1, T A Kent, C E Hulsebosch

  • 1Department of Anatomy, University of Texas Medical Branch, Galveston 77550-2772.

Neuroscience Letters
|November 23, 1992
PubMed
Summary

Central nervous system plasticity was investigated after cerebral ischemia. Studies show increased synaptophysin, indicating new synapse formation in the cortex surrounding infarction.

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Area of Science:

  • Neuroscience
  • Cerebrovascular Research
  • Neuroplasticity

Background:

  • Central nervous system plasticity is known after lesions but less studied post-cerebral ischemia.
  • Focal cerebral ischemia causes infarction surrounded by potentially reactive neuronal tissue.

Purpose of the Study:

  • To investigate synaptogenesis in the cortex following focal cerebral ischemia.
  • To assess changes in synapse number using synaptophysin immunoreactivity.

Main Methods:

  • Cerebral ischemia induced in hypertensive rats by occluding the middle cerebral artery and carotid artery.
  • Immunohistochemical techniques using antibodies to synaptophysin to measure synapse levels.
  • Comparison of synaptophysin immunoreactivity in the cortex adjacent to infarction versus the contralateral side.

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Main Results:

  • Statistically significant increase in anti-synaptophysin activity observed in the cortex surrounding the infarcted area.
  • This suggests a higher level of synaptophysin immunoreactivity on the side of the brain affected by ischemia.

Conclusions:

  • The increased synaptophysin immunoreactivity supports the hypothesis of synaptogenesis in the cortex post-cerebral infarction.
  • Findings indicate neuroplasticity occurs in the cortex following cerebral ischemia.