ALTERATION OF RYANODINE RECEPTOR IN THE HIPPOCAMPUS CA1 AFTER HEMISPHERIC CEREBRAL-ISCHEMIA

Citation
H. Nozaki et al., ALTERATION OF RYANODINE RECEPTOR IN THE HIPPOCAMPUS CA1 AFTER HEMISPHERIC CEREBRAL-ISCHEMIA, Neurochemical research, 21(8), 1996, pp. 975-982
Citations number
33
Categorie Soggetti
Biology,Neurosciences
Journal title
ISSN journal
03643190
Volume
21
Issue
8
Year of publication
1996
Pages
975 - 982
Database
ISI
SICI code
0364-3190(1996)21:8<975:AORRIT>2.0.ZU;2-8
Abstract
Alterations in ryanodine binding and local cerebral blood flow (LCBF) were examined at 30 minutes and 2 hours post-ischemia in the gerbil br ain in order to evaluate the influence of cerebral ischemia on the int racellular channels of Ca2+-induced Ca2+ release (CICR). Severe hemisp heric cerebral ischemia was induced by occluding the right common caro tid artery. LCBF was measured at the end of the experiment using [C-14 ]iodoantipyrine method, and the ryanodine binding was evaluated in vit ro using [H-3]ryanodine as a specific ligand for CICR channels. An aut oradiographic method developed in our laboratory enabled us to determi ne both parameters within the same brain. A group of gerbils who under went a sham procedure served as controls. LCBF was found to be signifi cantly reduced in most of the cerebral regions on the occluded side at both 30 minutes as well as 2 hours post-ischemia. In contrast, a sign ificant reduction in ryanodine binding was noted only in the hippocamp us CA1 on the occluded side at 30 minutes and 2 hours after the occlus ion These findings suggest that regionally specific changes of CICR ma y be the cause of decreased ryanodine binding in the hippocampus CA1, and that these changes may be related to the pathophysiological mechan isms that cause this region to be particularly vulnerable to ischemia.