Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Sustained elevation of calcium induces Ca2+/calmodulin-dependent protein kinase II clusters in hippocampal neurons
Autore:
Tao-Cheng, JH; Vinade, L; Smith, C; Winters, CA; Ward, R; Brightman, MW; Reese, TS; Dosemeci, A;
Indirizzi:
Marine Biol Lab, Woods Hole, MA 02543 USA Marine Biol Lab Woods Hole MA USA 02543 iol Lab, Woods Hole, MA 02543 USA NINCDS, Light Imaging Facil, NIH, Bethesda, MD 20892 USA NINCDS Bethesda MD USA 20892 t Imaging Facil, NIH, Bethesda, MD 20892 USA NINCDS, EM Facil, NIH, Bethesda, MD 20892 USA NINCDS Bethesda MD USA 20892 INCDS, EM Facil, NIH, Bethesda, MD 20892 USA NINCDS, Neurobiol Lab, NIH, Bethesda, MD 20892 USA NINCDS Bethesda MD USA20892 , Neurobiol Lab, NIH, Bethesda, MD 20892 USA
Titolo Testata:
NEUROSCIENCE
fascicolo: 1, volume: 106, anno: 2001,
pagine: 69 - 78
SICI:
0306-4522(2001)106:1<69:SEOCIC>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANSIENT CEREBRAL-ISCHEMIA; RAT-BRAIN INVIVO; CA1 REGION; TRANSLOCATION; PHOSPHORYLATION; CA-2+; FORM;
Keywords:
CaMKII clusters; hippocampal cultures; energy depletion; ischemia; excitotoxicity;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
22
Recensione:
Indirizzi per estratti:
Indirizzo: Dosemeci, A Marine Biol Lab, 7 MBL St, Woods Hole, MA 02543 USA Marine Biol Lab 7 MBL St Woods Hole MA USA 02543 MA 02543 USA
Citazione:
J.H. Tao-Cheng et al., "Sustained elevation of calcium induces Ca2+/calmodulin-dependent protein kinase II clusters in hippocampal neurons", NEUROSCIENC, 106(1), 2001, pp. 69-78

Abstract

Treatment of cultured hippocampal. neurons with the mitochondrial uncoupler carbonyl cyanide m-chlorophenylhydrazone (CCCP) in the absence of glucosemimics ischemic energy depletion and induces formation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) clusters, spherical structures with diameters of 75-175 nm [Dosemeci et al., J. Neurosci. 20 (2000) 3076-3084]. The demonstration that CaMKII clustering occurs in the intact, adult rat brain upon interruption of blood flow indicates that clustering is not confined to cell cultures. Application of N-methyl-Daspartate (250 muM, 15 min) tohippocampal cultures also induces cluster formation, suggesting a role forCa2+. Indeed, intracellular Ca2+ monitored with Fluo3-AM by confocal microscopy reaches a sustained high level within 5 min of CCCP treatment. The appearance of immunolabeled CaMKII clusters, detected by electron microscopy,follows the onset of the sustained increase in intracellular Ca2+. Moreover, CaMKII does not cluster when the rise in intracellular Ca2+ is preventedby the omission of extracellular Ca2+ during CCCP treatment, confirming that clustering is Ca2+-dependent. A lag period of 1-2 min between the onset of high intracellular Ca2+ levels and the formation of CaMKII clusters suggests that a sustained increase in Ca2+ level is necessary for the clustering. CaMKII clusters disappear within 2 h of returning the cultures to normalincubation conditions, at which time no significant cell death is detected. These results indicate that pathological conditions that promote sustainedepisodes of Ca2+ overload result in a transitory clustering of CaMKII intospherical structures. CaMKII clustering may represent a cellular defense mechanism to sequester a portion of the CaMKII pool, thereby preventing excessive protein phosphorylation. (C) 2001 IBRO. Published by Elsevier ScienceLtd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 01:07:09