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

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

STROKE, cilt.33, sa.5, ss.1369-1375, 2002 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 33 Sayı: 5
  • Basım Tarihi: 2002
  • Doi Numarası: 10.1161/01.str.0000013708.54623.de
  • Dergi Adı: STROKE
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.1369-1375
  • Anahtar Kelimeler: 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
  • Ankara Üniversitesi Adresli: Evet

Özet

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.