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Titolo:
Modulation of calcium-evoked [H-3]noradrenaline release from permeabilizedcerebrocortical synaptosomes by the MARCKS protein, calmodulin and the actin cytoskeleton
Autore:
Walaas, SI; Sefland, I;
Indirizzi:
Univ Oslo, Inst Basic Med Sci, Neurochem Lab, N-0317 Oslo, Norway Univ Oslo Oslo Norway N-0317 Med Sci, Neurochem Lab, N-0317 Oslo, Norway
Titolo Testata:
NEUROCHEMISTRY INTERNATIONAL
fascicolo: 7, volume: 36, anno: 2000,
pagine: 581 - 593
SICI:
0197-0186(200006)36:7<581:MOC[RF>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
KINASE-C SUBSTRATE; ISOLATED NERVE-TERMINALS; I-DEFICIENT MICE; NEUROTRANSMITTER RELEASE; CHROMAFFIN CELLS; NORADRENALINE RELEASE; SYNAPTIC VESICLES; SYNAPSIN-I; GLUTAMATE RELEASE; STREPTOLYSIN-O;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
83
Recensione:
Indirizzi per estratti:
Indirizzo: Walaas, SI Univ Oslo, Inst Basic Med Sci, Neurochem Lab, POB 1115,Blindern, N-0317 Oslo, Norway Univ Oslo POB 1115,Blindern Oslo Norway N-0317 17 Oslo, Norway
Citazione:
S.I. Walaas e I. Sefland, "Modulation of calcium-evoked [H-3]noradrenaline release from permeabilizedcerebrocortical synaptosomes by the MARCKS protein, calmodulin and the actin cytoskeleton", NEUROCHEM I, 36(7), 2000, pp. 581-593

Abstract

In order to examine intracellular modulation of CNS catecholamine release,cerebrocortical synaptosomes were prelabeled with [H-3]noradrenaline and permeabilized with streptolysin-O in the absence or presence of Ca2+. Plasmamembrane permeabilization allowed efflux of cytosol and left a compartmentalized pool of [H-3]noradrenaline intact, approximately 10% of which was released by addition of 10(-5) M Ca2+. Addition of activators or inhibitors of protein kinase C, as well as inhibitors of Ca2+-calmodulin kinase II or calcineurin, failed to change Ca2+-induced noradrenaline release. Evoked release from permeabilized synaptosomes deficient in the vesicle-associated phosphoprotein synapsin I was also unchanged. In contrast, addition of a synthetic 'active domain' peptide from the myristoylated, alanine-rich C-kinasesubstrate (MARCKS) protein increased, while addition of calmodulin decreased Ca2+-induced release from the permeabilized synaptosomes, the latter effect being reversed by a peptide inhibitor of calcineurin. Moreover, addition of the actin-destabilizing agent DNase I, as well as antibodies to MARCKS, appeared to increase spontaneous, Ca2+-independent release from noradrenergic vesicles. These results indicate that the MARCKS protein may modulate release from permeabilized noradrenergic synaptosomes, possibly by modulating calmodulin levels and/or the actin cytoskeleton. (C) 2000 Elsevier Science Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/04/20 alle ore 18:40:48