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Titolo:
Selective inhibition of inositol 1,4,5-trisphosphate-induced Ca2+ release in the CA1 region of the hippocampus in the ischemic gerbil
Autore:
Nagata, E; Tanaka, K; Suzuki, S; Dembo, T; Fukuuchi, Y; Futatsugi, A; Mikoshiba, K;
Indirizzi:
Keio Univ, Sch Med, Dept Neurol, Shinjuku Ku, Tokyo 1608582, Japan Keio Univ Tokyo Japan 1608582 Neurol, Shinjuku Ku, Tokyo 1608582, Japan RIKEN, Inst Phys & Chem Res, Brain Sci Inst, Dev Neurobiol Lab, Wako, Saitama, Japan RIKEN Wako Saitama Japan i Inst, Dev Neurobiol Lab, Wako, Saitama, Japan Univ Tokyo, Inst Med Sci, Dept Mol Neurobiol, Tokyo, Japan Univ Tokyo Tokyo Japan , Inst Med Sci, Dept Mol Neurobiol, Tokyo, Japan ERATO, Calsiosignal Net Project, Tokyo, Japan ERATO Tokyo JapanERATO, Calsiosignal Net Project, Tokyo, Japan
Titolo Testata:
NEUROSCIENCE
fascicolo: 3, volume: 93, anno: 1999,
pagine: 995 - 1001
SICI:
0306-4522(1999)93:3<995:SIOI1C>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
CEREBELLAR PURKINJE-CELLS; NEURONAL DEATH; CATHEPSIN-B; RYANODINE RECEPTOR; CALCIUM POOLS; BRAIN; EXPRESSION; DEGRADATION; CHANNELS; CALPAINS;
Keywords:
inositol 1,4,5-trisphosphate receptor; brain ischemia; Ca2+ mobilization; endoplasmic reticulum; stack phenomenon; CA1region of the hippocampus;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Tanaka, K Keio Univ, Sch Med, Dept Neurol, Shinjuku Ku, 35 Shinanomachi, Tokyo 1608582, Japan Keio Univ 35 Shinanomachi Tokyo Japan 1608582 yo 1608582, Japan
Citazione:
E. Nagata et al., "Selective inhibition of inositol 1,4,5-trisphosphate-induced Ca2+ release in the CA1 region of the hippocampus in the ischemic gerbil", NEUROSCIENC, 93(3), 1999, pp. 995-1001

Abstract

We examined the effect of ischemia on inositol 1,4,5-trisphosphate receptor-induced Ca2+ release by functional and morphological approaches, using the gerbil model after 6-h unilateral occlusion of the common carotid artery. Autoradiographic study revealed that the basal uptake of Ca-45(2+) into the endoplasmic reticulum and caffeine-induced Ca-45(2+) release from the endoplasmic reticulum were normal in the presence of ATP in each ischemic brain region, whereas inositol 1,4,5-trisphosphate receptor-induced Ca-45(2+) release from the endoplasmic reticulum was inhibited only in the CAI region of the hippocampus on the ischemic side. In moderately ischemic gerbils, electron microscopic study demonstrated aggregation of swollen endoplasmic reticulum in the CAI region of the hippocampus, so that abundant endoplasmic reticulum assembled in close contact to form endoplasmic reticulum cisternal stacks. In severely ischemic gerbils, immunohistochemical analysis of thehippocampus showed loss of type 1 inositol 1,4,5-trisphosphate receptor protein with preservation of immunoreactivity for type 2 and 3 inositol 1,4,5-trisphosphate receptor proteins, which was confirmed by western blot analysis. Such selective inhibition of inositol 1,4,5-trisphosphate receptor-inducedCa2+ release and the loss of type 1 inositol 1,4,5 trisphosphate receptor in the CA1 region of the hippocampus in cerebral ischemia may be associatedwith its region-specific vulnerability to ischemia. (C) 1999 IBRO. Published by Elsevier Science Ltd.

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Documento generato il 11/07/20 alle ore 14:34:00