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Titolo:
Global ischemia-induced increases in the gap junctional proteins connexin 32 (Cx32) and Cx36 in hippocampus and enhanced vulnerability of Cx32 knock-out mice
Autore:
Oguro, K; Jover, T; Tanaka, H; Lin, Y; Kojima, T; Oguro, N; Grooms, SY; Bennett, MVL; Zukin, RS;
Indirizzi:
Albert Einstein Coll Med, Dept Neurosci, Bronx, NY 10461 USA Albert Einstein Coll Med Bronx NY USA 10461 Neurosci, Bronx, NY 10461 USA
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 19, volume: 21, anno: 2001,
pagine: 7534 - 7542
SICI:
0270-6474(20011001)21:19<7534:GIIITG>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
DELAYED NEURONAL DEATH; RAT-BRAIN; FOREBRAIN ISCHEMIA; GERBIL HIPPOCAMPUS; GENE-EXPRESSION; INFARCT VOLUME; RNA ISOLATION; CELL-DEATH; RETINA; ASTROCYTES;
Keywords:
gap junctions; neural connexins; global ischemia; neuronal death; GABAergic interneurons; electrical transmission; Cx32 knock-out;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
58
Recensione:
Indirizzi per estratti:
Indirizzo: Bennett, MVL Albert Einstein Coll Med, Dept Neurosci, 1300 Morris Pk Ave, Bronx, NY 10461 USA Albert Einstein Coll Med 1300 Morris Pk Ave Bronx NY USA 10461
Citazione:
K. Oguro et al., "Global ischemia-induced increases in the gap junctional proteins connexin 32 (Cx32) and Cx36 in hippocampus and enhanced vulnerability of Cx32 knock-out mice", J NEUROSC, 21(19), 2001, pp. 7534-7542

Abstract

Gap junctions are conductive channels that connect the interiors of coupled cells. In the hippocampus, GABA-containing hippocampal interneurons are interconnected by gap junctions, which mediate electrical coupling and synchronous firing and thereby promote inhibitory transmission. The present study was undertaken to examine the hypothesis that the gap junctional proteinsconnexin 32 (Cx32; expressed by oligodendrocytes, interneurons, or both), Cx36 (expressed by interneurons), and Cx43 (expressed by astrocytes) play arole in defining cell-specific patterns of neuronal death in hippocampus after global ischemia in mice. Global ischemia did not significantly alter Cx32 and Cx36 mRNA expression and slightly increased Cx43 mRNA expression inthe vulnerable CA1, as assessed by Northern blot analysis and in situ hybridization. Global ischemia induced a selective increase in Cx32 and Cx36 but not Cx43 protein abundance in CA1 before onset of neuronal death, as assessed by Western blot analysis. The increase in Cx32 and Cx36 expression wasintense and specific to parvalbumin-positive inhibitory interneurons of CA1, as assessed by double immunofluorescence. Protein abundance was unchanged in CA3 and dentate gyrus. The finding of increase in connexin protein without increase in mRNA suggests regulation of Cx32 and Cx36 expression at the translational or post-translational level. Cx32(Y/-) null mice exhibited enhanced vulnerability to brief ischemic insults, consistent with a role for Cx32 gap junctions in neuronal survival. These findings suggest that Cx32and Cx36 gap junctions may contribute to the survival and resistance of GABAergic interneurons, thereby defining cell-specific patterns of global ischemia-induced neuronal death.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 07/07/20 alle ore 19:03:51