Increase in synaptophysin immunoreactivity following cortical infarction

R. Paul Stroemer, Thomas A. Kent, Claire E. Hulsebosch

Research output: Contribution to journalArticlepeer-review

35 Scopus citations


Plasticity in the central nervous system has been demonstrated using lesions of the hippocampus and rhinal cortex but has not been well studied after cerebral ischemia. Focal cerebral ischemia creates an area of infarction that is surrounded by neuronal tissue that may respond to nearby damage by creating new synapses. To determine if synaptogenesis occurs, antibodies to synaptophysin, a calcium-binding protein found on synaptic vesicles, were used with immunohistochemical techniques to assess the level of synaptophysin immunoreactivity as a measure of changes in the number of synapses. Cerebral ischemia was induced in hypertensive rats by permanently occluding the distal middle cerebral artery and ipsilateral common carotid artery. After 2 months recovery, the animals were perfused and the brains removed for immunohistochemical processing and evaluation. When comparing the cortex surrounding the infarcted area to similar areas on the contralateral side of the brain, the infarcted side had increased levels of anti-synaptophysin like activity that are statistically significant. We hypothesize that this increase in synaptophysin immunoreactivity is due to an increase in synapses in the cortex surrounding an area of infarction and supports the hypothesis of plasticity in the cortex following cerebral infarction.

Original languageEnglish (US)
Pages (from-to)21-24
Number of pages4
JournalNeuroscience Letters
Issue number1
StatePublished - Nov 23 1992


  • Cerebral ischemia
  • Immunohistochemistry
  • Middle cerebral artery
  • Plasticity
  • Synaptogenesis
  • Synaptophysin

ASJC Scopus subject areas

  • Neuroscience(all)


Dive into the research topics of 'Increase in synaptophysin immunoreactivity following cortical infarction'. Together they form a unique fingerprint.

Cite this