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Titolo:
Nitric oxide directly activates GABA(A) receptor function through a cGMP/protein kinase-independent pathway in frog pituitary melanotrophs
Autore:
Castel, H; Vaudry, H;
Indirizzi:
Univ Rouen, European Inst Peptide Res IFRMP 23, Lab Cellular & Mol Neuroendocrinol, UA CNRS,INSERM,U413, F-76821 Mont St Aignan, France Univ Rouen Mont St Aignan France F-76821 F-76821 Mont St Aignan, France
Titolo Testata:
JOURNAL OF NEUROENDOCRINOLOGY
fascicolo: 8, volume: 13, anno: 2001,
pagine: 695 - 705
SICI:
0953-8194(200108)13:8<695:NODAGR>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
GAMMA-AMINOBUTYRIC-ACID; RETINAL GANGLION-CELLS; UNION-OF-PHARMACOLOGY; NMDA RECEPTOR; A RECEPTORS; SULFHYDRYL-GROUPS; REDOX MODULATION; XENOPUS-LAEVIS; ION CHANNELS; SUBUNIT;
Keywords:
nitric oxide donor; gamma-aminobutyric acid type A receptor; redox site; S-nitrosylation; sulfhydryl-modifying agent; patch-clamp; inside-out;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Vaudry, H Univ Rouen, European Inst Peptide Res IFRMP 23, Lab Cellular & Mol Neuroendocrinol, UA CNRS,INSERM,U413, F-76821 Mont St Aignan, France Univ Rouen Mont St Aignan France F-76821 ont St Aignan, France
Citazione:
H. Castel e H. Vaudry, "Nitric oxide directly activates GABA(A) receptor function through a cGMP/protein kinase-independent pathway in frog pituitary melanotrophs", J NEUROENDO, 13(8), 2001, pp. 695-705

Abstract

The direct effects of nitric oxide (NO) donors and sulfhydryl-modifying agents on the GABA(A) receptor function were examined by perforated patch, whole-cell and single channel recordings in cultured frog melanotrophs. In amphotericin B-perforated cells incubated with the soluble guanylyl cyclase inhibitors LY 83583 and ODQ (10(-4) M each), the NO donor sodium nitroprusside (SNP) (10(-3) M) reversibly increased the current evoked by GABA (5 x 10(-6) M). In the whole-cell configuration, internal application of the oxidizing agent H2O2 (0.05%) potentiated the GABA-evoked current while the reducing agent 2-mercaptoethanol (5 x 10(-3) M) slightly decreased the current amplitude. In inside-out patches, GABA (2 x 10(-7) M) triggered single channel bursts of openings. Incubation with the NO donors SNP or DEA/NO (10(-4) M each) enhanced the open probability of the GABA(A) receptor channel but did not modify the chloride reversal potential and did not affect the conductance states. The oxidizing agents H2O2 (0.05%) or DTNB (10(-4) M) mimickedthe stimulatory effect of the NO donors on the open probability while the reducing Compounds 2-mercaptoethanol (5 x 10(-3) M) or DTT (10(-4) M) markedly attenuated the channel activity. Potentiation of the GABA-induced single channel activity by SNP or H2O2 was blocked by 2-mercaptoethanol. Similarly, the potentiating effect produced by DEA/NO or DTNB on the open probability was reversed by DTT. In outside-out patches, incubation with SNP also significantly enhanced the open probability of single channels activated by GABA (10(-6) M). These data indicate that, in frog pituitary melanotrophs, NO potentiates the GABA-evoked current independently of the cGMP/protein kinase pathway. The effect of NO can be accounted for by S-nitrosylation/oxidation of thiol groups either directly on the GABA(A) receptor subunits or on a regulatory protein tightly associated with the GABA(A) receptor.

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Documento generato il 06/04/20 alle ore 23:35:10