Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
DESIPRAMINE MODULATES H-3 OUABAIN BINDING IN RAT HYPOTHALAMUS
Autore:
VIOLA MS; ANTONELLI MC; ENERO MA; ARNAIZ GRD;
Indirizzi:
UNIV BUENOS AIRES,FAC MED,INST BIOL CELULAR & NEUROCIENCIAS PROF EDUARDO DE RA-1121 BUENOS AIRES DF ARGENTINA UNIV BUENOS AIRES,FAC MED,INST BIOL CELULAR & NEUROCIENCIAS PROF EDUARDO DE RA-1121 BUENOS AIRES DF ARGENTINA UNIV BUENOS AIRES,FAC FARM & BIOQUIM,CATEDRA FARMACOL RA-1121 BUENOS AIRES DF ARGENTINA
Titolo Testata:
Journal of neuroscience research
fascicolo: 1, volume: 47, anno: 1997,
pagine: 77 - 82
SICI:
0360-4012(1997)47:1<77:DMHOBI>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
QUANTITATIVE AUTORADIOGRAPHY; NA+/K+-ATPASE; PLASMA-MEMBRANE; SKELETAL-MUSCLE; HIGH-AFFINITY; OUABAIN; BRAIN; TRANSLOCATION; LOCALIZATION; IMIPRAMINE;
Keywords:
TRICYCLIC ANTIDEPRESSANTS; OUABAIN BINDING; K+ P-NPPASE; DESIPRAMINE; QUANTITATIVE AUTORADIOGRAPHY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
30
Recensione:
Indirizzi per estratti:
Citazione:
M.S. Viola et al., "DESIPRAMINE MODULATES H-3 OUABAIN BINDING IN RAT HYPOTHALAMUS", Journal of neuroscience research, 47(1), 1997, pp. 77-82

Abstract

We have previously shown that Na+, K+-ATPase activity in hypothalamusis increased after administration of an acute dose of desipramine, a noradrenaline uptake inhibitor (Viola et al., Cell Molec Neurobiol 9:263-271, 1989). In this report the same treatment (10 mg per kg) was applied to evaluate H-3-ouabain binding in rat brain sections by quantitative autoradiography, Results disclosed an increase in the number of ouabain binding sites in hypothalamus but not in cerebral cortex, Concomitantly, such acute DMI treatment enhanced K+-stimulated-p-nitrophenylphosphatase activity in hypothalamus membranes whereas it failed to modify cerebral cortex membranes, A direct interaction of DMI with theenzyme was ruled out since in vitro DMI is known to inhibit the enzyme, It may be speculated that DMI indirectly stimulates Na+, K+-ATPase through the increase in noradrenaline which acts in turn on the external phosphorylated site of the enzyme. (C) 1997 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/09/20 alle ore 04:55:24