Persistent defect in transmitter release and synapsin phosphorylation in cerebral cortex after transient moderate ischemic injury

Bolay H. B., Gursoy-Ozdemir Y., Sara Y., Onur R., Can A., Dalkara T.

STROKE, vol.33, no.5, pp.1369-1375, 2002 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 33 Issue: 5
  • Publication Date: 2002
  • Doi Number: 10.1161/01.str.0000013708.54623.de
  • Journal Name: STROKE
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.1369-1375
  • Keywords: cerebral ischemia, focal, motor cortex, phosphorylation, proteins, somatosensory cortex, synapses, rats, DEPENDENT PROTEIN-KINASE, RAT MOTOR CORTEX, POSTSYNAPTIC DENSITIES, SYNAPTIC TRANSMISSION, HIPPOCAMPAL SLICES, CORTICAL SYNAPSES, MAJOR DETERMINANT, ARTERY OCCLUSION, FOCAL ISCHEMIA, MCA OCCLUSION
  • Gazi University Affiliated: Yes

Abstract

Background and Purpose-Synaptic transmission is highly vulnerable to metabolic perturbations. However, the long-term consequences of transient metabolic perturbations on synapses are not clear. We studied the long-lasting changes in synaptic transmission and phosphorylation of presynaptic proteins in penumbral cortical neurons after transient moderate ischemia.