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.
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Authors | Dimitrula Arabadzisz, Aarne Ylinen, Zsuzsa Emri |
Journal | Neuroscience letters
(Neurosci Lett)
Vol. 331
Issue 2
Pg. 103-6
(Oct 11 2002)
ISSN: 0304-3940 [Print] Ireland |
PMID | 12361851
(Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Calbindins
- S100 Calcium Binding Protein G
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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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