H. Nozaki et al., ALTERATION OF RYANODINE RECEPTOR IN THE HIPPOCAMPUS CA1 AFTER HEMISPHERIC CEREBRAL-ISCHEMIA, Neurochemical research, 21(8), 1996, pp. 975-982
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.