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Titolo:
Control of astrocyte Ca2+ oscillations and waves by oscillating translocation and activation of protein kinase C
Autore:
Codazzi, F; Teruel, MN; Meyer, T;
Indirizzi:
Stanford Univ, Med Ctr, Dept Mol Pharmacol, Stanford, CA 94305 USA Stanford Univ Stanford CA USA 94305 Mol Pharmacol, Stanford, CA 94305 USA San Raffaele Sci Inst, Dept Neurosci, Dibit, I-20132 Milan, Italy San Raffaele Sci Inst Milan Italy I-20132 i, Dibit, I-20132 Milan, Italy
Titolo Testata:
CURRENT BIOLOGY
fascicolo: 14, volume: 11, anno: 2001,
pagine: 1089 - 1097
SICI:
0960-9822(20010724)11:14<1089:COACOA>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
GREEN FLUORESCENT PROTEIN; INTERNAL-REFLECTION FLUORESCENCE; METABOTROPIC GLUTAMATE RECEPTORS; CALCIUM WAVES; INOSITOL 1,4,5-TRISPHOSPHATE; CULTURED ASTROCYTES; CYTOSOLIC CA2+; BINDING DOMAIN; PHORBOL ESTER; LIVING CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Meyer, T Stanford Univ, Med Ctr, Dept Mol Pharmacol, 269 Campus Dr, Stanford, CA 94305 USA Stanford Univ 269 Campus Dr Stanford CA USA 94305 d, CA 94305 USA
Citazione:
F. Codazzi et al., "Control of astrocyte Ca2+ oscillations and waves by oscillating translocation and activation of protein kinase C", CURR BIOL, 11(14), 2001, pp. 1089-1097

Abstract

Background: Glutamate-induced Ca2+ oscillations and waves coordinate astrocyte signaling responses, which in turn regulate neuronal excitability. Recent studies have suggested that the generation of these Ca2+ oscillations requires a negative feedback that involves the activation of conventional protein kinase C (cPKC). Here, we use total internal reflection fluorescence (TIRF) microscopy to investigate if and how periodic plasma membrane translocation of cPKC is used to generate Ca2+ oscillations and waves. Results: Glutamate stimulation of astrocytes triggered highly localized GFP-PKC gamma plasma membrane translocation events, induced rapid oscillations in GFP-PKC gamma translocation, and generated GFP-PKC gamma translocationwaves that propagated across and between cells. These translocation responses were primarily mediated by the Ca2+-sensitive C2 domains of PKC gamma and were driven by localized Ca2+ spikes, by oscillations in Ca2+ concentration, and by propagating Ca2+ waves, respectively. Interestingly, GFP-conjugated C1 domains from PKC gamma or PKC delta that have been shown to bind diacylglycerol (DAG) also oscillated between the cytosol and the plasma membrane after glutamate stimulation, suggesting that PKC is repetitively activated by combined oscillating increases in Ca2+ and DAG concentrations. The expression of C1 domains, which increases the DAG buffering capacity and thereby delays changes in DAG concentrations, led to a marked prolongation of Ca2+ spikes, suggesting that PKC activation is involved in terminating individual Ca2+ spikes and waves and in defining the time period between Ca2+ spikes. Conclusions: Our study suggests that cPKCs have a negative feedback role on Ca2+ oscillations and waves that is mediated by their repetitive activation by oscillating DAG and Ca2+ concentrations. Periodic translocation and activation of cPKC can be a rapid and markedly localized signaling event that can limit the duration of individual Ca2+ spikes and waves and can definethe Ca2+ spike and wave frequencies.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/03/20 alle ore 23:21:32