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Increased inter-spike intervals and fast after-hyperpolarization of action potentials in rat hippocampal pyramidal cells accompanied with altered calbindin immunoreactivity 10-12 months after global forebrain ischemia.

Abstract
In vivo electrophysiological recordings of CA1/CA2 pyramidal cells were performed 10-12 months after global forebrain ischemia (four-vessel occlusion, 15 mm) and were compared to levels of calbindin expression. Ischemic animals were subdivided in non-sclerotic ischemic (NSI) and sclerotic ischemic (SI) groups depending on the absence or presence of hippocampal sclerosis. A decreased excitability was observed in neurons from both groups, as shown by significant prolongation of inter-spike intervals (ISI) of evoked action potentials and by increased amplitude of fast after-hyperpolarization (fAHP). The ratio of calbindin-positive CA1/CA2 pyramidal cells decreased from 59% in control to 33% and 8% in NSI and SI animals, respectively. These results suggest that decreased excitability of CA1/CA2 pyramidal cells represents a protective mechanism against ischemia-induced neurodegeneration and might be related to decreased calbindin expression.
AuthorsDimitrula Arabadzisz, Aarne Ylinen, Zsuzsa Emri
JournalNeuroscience letters (Neurosci Lett) Vol. 331 Issue 2 Pg. 103-6 (Oct 11 2002) ISSN: 0304-3940 [Print] Ireland
PMID12361851 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Calbindins
  • S100 Calcium Binding Protein G
Topics
  • Animals
  • Calbindins
  • Electrophysiology
  • Evoked Potentials (physiology)
  • Hypoxia-Ischemia, Brain (metabolism, pathology)
  • Male
  • Pyramidal Cells (metabolism)
  • Rats
  • Rats, Wistar
  • S100 Calcium Binding Protein G (biosynthesis)
  • Sclerosis
  • Time Factors

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