Post-ischemic changes of [3H]glycine binding in the gerbil brain after cerebral ischemia.
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.
Araki
T
T
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.
Kato
H
H
Fujiwara
T
T
Kogure
K
K
Itoyama
Y
Y
D000818:Animals; D000911:Antibodies, Monoclonal; D001345:Autoradiography; D001921:Brain / Q000378:metabolism* / Q000473:pathology; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology; D005849:Gerbillinae; D005998:Glycine / Q000378:metabolism*; D007150:Immunohistochemistry; D008297:Male; D018009:Receptors, Glycine / Q000378:metabolism
D000911:Antibodies, Monoclonal; D018009:Receptors, Glycine; D005998:Glycine