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Titolo:
Role of the ryanodine receptor in ischemic brain damage - Localized reduction of ryanodine receptor binding during ischemia in hippocampus CA1
Autore:
Nozaki, H; Tanaka, K; Gomi, S; Mihara, B; Nogawa, S; Nagata, E; Kondo, T; Fukuuchi, Y;
Indirizzi:
Keio Univ, Sch Med, Dept Neurol, Shinjuku Ku, Tokyo 1608582, Japan Keio Univ Tokyo Japan 1608582 Neurol, Shinjuku Ku, Tokyo 1608582, Japan Mihara Mem Hosp, Gunma 372, Japan Mihara Mem Hosp Gunma Japan 372Mihara Mem Hosp, Gunma 372, Japan
Titolo Testata:
CELLULAR AND MOLECULAR NEUROBIOLOGY
fascicolo: 1, volume: 19, anno: 1999,
pagine: 119 - 131
SICI:
0272-4340(199902)19:1<119:ROTRRI>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
CALCIUM-RELEASE CHANNEL; MUSCLE SARCOPLASMIC-RETICULUM; CYCLIC ADP-RIBOSE; INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR; DELAYED NEURONAL DEATH; CEREBRAL BLOOD-FLOW; FREE FATTY-ACIDS; SKELETAL-MUSCLE; CA2+ RELEASE; GERBIL BRAIN;
Keywords:
ryanodine receptor; cerebral ischemia; second messenger; Ca2+;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
64
Recensione:
Indirizzi per estratti:
Indirizzo: Nozaki, H Keio2,niv, Sch Med, Dept Neurol, Shinjuku Ku, 35 Shinanomachi, Tokyo 160858 Keio Univ 35 Shinanomachi Tokyo Japan 1608582 chi, Tokyo 160858
Citazione:
H. Nozaki et al., "Role of the ryanodine receptor in ischemic brain damage - Localized reduction of ryanodine receptor binding during ischemia in hippocampus CA1", CELL MOL N, 19(1), 1999, pp. 119-131

Abstract

1. The ryanodine receptor has recently been shown to play a pivotal role in the regulation of intracellular Ca2+ concentration via Call-induced Ca2+ release (CICR). Effects of ischemia on CICR in the brain tissue, however, remain largely unknown since only a few reports have been published on this subject. In this paper we report on work in this area by our group and review related progress in this field.2. We examined alterations of ryanodine receptor binding and local cerebral blood how (LCBF) at 15 min, 30 min, and 2 hr after occlusion of the rightcommon carotid artery in the gerbil brain. A quantitative autoradiographicmethod permitted simultaneous measurement of these parameters in the same brain. The LCBF was significantly reduced in most of the cerebral regions on the occluded side during each time period of ischemia. In contrast, only in the hippocampus CA 1 on the occluded side was a significant reduction inryanodine binding found at 15 min, 30 min and 2 hr after the occlusion.3. These findings suggest that suppression of ryanodine binding in the hippocampus CA1 may be attributable to a regionally specific perturbation of CICR and that this perturbation may be closely associated with the pathophysiological mechanism that leads to the selective ischemic vulnerability of this region.4. Other recent studies have also reported an important role for ryanodinereceptors in neuronal injury such as the delayed neuronal death in the hjppocampus CA1. These data suggest that derangement of CICR is likely to be involved in acute neuronal necrosis as well as in delayed neuronal death in ischemia.5. Further studies on clarifying the role of CICR in ischemic brain damageare needed in order to develop new therapeutic strategies for stroke patients.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/07/20 alle ore 01:13:14