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Post-ischemic changes of [3H]glycine binding in the gerbil brain after cerebral ischemia.

Abstract
Sequential changes of [3H]glycine binding in the gerbil were investigated in selectively vulnerable areas 1 h to 7 days after 10 min of cerebral ischemia. A significant reduction in [3H]glycine binding was found in the hippocampus and thalamus from as early as 1 h after ischemia. In contrast, the striatum and frontal cortex showed a significant decline in [3H]glycine binding from 5 h after recirculation. Thereafter, a severe reduction in [3H]glycine binding was observed in all regions 7 days after ischemia. MAP2 (microtubule-associated protein 2) immunoreactivity was unaffected in the hippocampus, frontal cortex and thalamus up to 48 h after ischemia. Thereafter, a severe loss of MAP2-immunoreactive neurons was found in these regions, especially in the hippocampal CA1 sector. However, the striatum showed a severe loss of MAP2 immunoreactivity from 24 h after ischemia. These results demonstrate that transient cerebral ischemia causes severe reduction in [3H]glycine binding throughout the brain, and this reduction precedes the neuronal damage in selectively vulnerable areas. These findings suggest that a neurotransmitter, glycine, may play a key role in the pathogenesis of post-ischemic neurodegeneration in selectively vulnerable areas.
AuthorsT Araki, H Kato, T Fujiwara, K Kogure, Y Itoyama
JournalEuropean journal of pharmacology (Eur J Pharmacol) Vol. 278 Issue 2 Pg. 91-6 (May 15 1995) ISSN: 0014-2999 [Print] Netherlands
PMID7672005 (Publication Type: Journal Article)
Chemical References
  • Antibodies, Monoclonal
  • Receptors, Glycine
  • Glycine
Topics
  • Animals
  • Antibodies, Monoclonal
  • Autoradiography
  • Brain (metabolism, pathology)
  • Brain Ischemia (metabolism, pathology)
  • Gerbillinae
  • Glycine (metabolism)
  • Immunohistochemistry
  • Male
  • Receptors, Glycine (metabolism)

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