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Titolo:
NITRIC-OXIDE INHIBITS HYPOTHALAMIC LUTEINIZING-HORMONE-RELEASING HORMONE-RELEASE BY RELEASING GAMMA-AMINOBUTYRIC-ACID
Autore:
SEILICOVICH A; DUVILANSKI BH; PISERA D; THEAS S; GIMENO M; RETTORI V; MCCANN SM;
Indirizzi:
UNIV TEXAS,SW MED CTR,DEPT PHYSIOL,DIV NEUROPEPTIDE,5323 HARRY HINES BLVD DALLAS TX 75235 UNIV TEXAS,SW MED CTR,DEPT PHYSIOL,DIV NEUROPEPTIDE DALLAS TX 75235 UNIV BUENOS AIRES,FAC MED,CTR INVEST REPROD RA-1121 BUENOS AIRES DF ARGENTINA CONSEJO NACL INVEST CIENT & TECN,CTR ESTUDIOS FARMACOL & BOT RA-1414 BUENOS AIRES DF ARGENTINA
Titolo Testata:
Proceedings of the National Academy of Sciences of the United Statesof America
fascicolo: 8, volume: 92, anno: 1995,
pagine: 3421 - 3424
SICI:
0027-8424(1995)92:8<3421:NIHLH>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
GABA; SECRETION; RAT;
Keywords:
IN VITRO MEDIAL BASAL HYPOTHALAMIC EXPLANTS; SODIUM NITROPRUSSIDE; HEMOGLOBIN; N-G-MONOMETHYL-L ARGININE; HIGH K+ MEDIUM;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
25
Recensione:
Indirizzi per estratti:
Citazione:
A. Seilicovich et al., "NITRIC-OXIDE INHIBITS HYPOTHALAMIC LUTEINIZING-HORMONE-RELEASING HORMONE-RELEASE BY RELEASING GAMMA-AMINOBUTYRIC-ACID", Proceedings of the National Academy of Sciences of the United Statesof America, 92(8), 1995, pp. 3421-3424

Abstract

Nitric oxide synthase (NOS) containing neurons, termed NOergic neurons, occur in various regions of the hypothalamus, including the median eminence-arcuate region, which plays an important role in controlling the release of luteinizing hormone-releasing hormone (LHRH). We examined the effect of NO on release of gamma-aminobutyric acid (GABA) from medial basal hypothalamic (MBH) explants incubated in vitro. Sodium nitroprusside (NP) (300 mu M), a spontaneous releaser of NO, doubled therelease of GABA. This release was significantly reduced by incubationof the tissue with hemoglobin, a scavenger of NO, whereas hemoglobin alone had no effect on the basal release of GABA. Elevation of the potassium concentration (40 mM) in the medium increased GABA release 15-fold; this release was further augmented by NP. Hemoglobin blocked the increase in GABA release induced by NP but had no effect on potassium-induced release, suggesting that the latter is not related to NO. As in the case of hemoglobin, N-G-monomethyl-L-arginine (NMMA), a competitive inhibitor of NOS, had no effect on basal release of GABA, which indicates again that NO is not significant to basal GABA release. However, NMMA markedly inhibited the release of GABA induced by high potassium, which indicates that NO plays a role in potassium-induced release of GABA. In conditions in which the release of GABA was substantially augmented, there was a reduction in GABA tissue stores as well, suggesting that synthesis of GABA in these conditions did not keep up with release of the amine. Although NO released GABA, there was no effect ofthe released GABA on NO production, for incubation of MBH explants with GABA had no effect on NO release as measured by [C-14]citrulline production. To determine whether GABA had any effect on the release of LHRH from these MBH explants, GABA was incubated with the tissue and the effect on LHRH release was determined. GABA (10(-5) or 10(-6) M) induced a 70% decrease in the release of LHRH, indicating that in the male rat GABA inhibits the release of this hypothalamic peptide. This inhibition in LHRH release induced by GABA was blocked by NMMA (300 mu M), which indicates that GABA converts the stimulatory effect of NO on LHRH release into an inhibitory one, presumably via GABA receptors, which activate chloride channels that hyperpolarize the cell. Previous results have indicated that norepinephrine stimulates release of NO fromthe NOergic neurons, which then stimulates the release of LHRH. The current results indicate that the NO released also induces release of GABA, which then inhibits further LHRH release. Thus, in vivo the norepinephrinergic-driven pulses of LHRH release may be terminated by GABA released from GABAergic neurons via NO.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 22:43:14