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Titolo:
MAGNESIUM AND ZINC POTENTIATE ETHANOL INHIBITION OF N-METHYL-D-ASPARTATE-STIMULATED NITRIC-OXIDE SYNTHASE IN CORTICAL-NEURONS
Autore:
CHANDLER LJ; GUZMAN NJ; SUMNERS C; CREWS FT;
Indirizzi:
LOUISIANA STATE UNIV,MED CTR,DEPT PHARMACOL & THERAPEUT,1501 KINGS HIGHWAY SHREVEPORT LA 71130 UNIV FLORIDA,COLL MED,DEPT PHARMACOL GAINESVILLE FL 00000 UNIV FLORIDA,COLL MED,DEPT PHYSIOL GAINESVILLE FL 00000
Titolo Testata:
The Journal of pharmacology and experimental therapeutics
fascicolo: 1, volume: 271, anno: 1994,
pagine: 67 - 75
SICI:
0022-3565(1994)271:1<67:MAZPEI>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
LONG-TERM POTENTIATION; NMDA-RECEPTOR; NADPH-DIAPHORASE; RAT-BRAIN; INTERCELLULAR MESSENGER; HUNTINGTONS-DISEASE; HIPPOCAMPAL SLICE; MOLECULAR-CLONING; RELEASE; CHANNELS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
52
Recensione:
Indirizzi per estratti:
Citazione:
L.J. Chandler et al., "MAGNESIUM AND ZINC POTENTIATE ETHANOL INHIBITION OF N-METHYL-D-ASPARTATE-STIMULATED NITRIC-OXIDE SYNTHASE IN CORTICAL-NEURONS", The Journal of pharmacology and experimental therapeutics, 271(1), 1994, pp. 67-75

Abstract

The coupling of calcium mobilizing receptors to nitric oxide (NO) formation was examined in cerebral cortical cultures. Of the various agents tested, only glutamate, depolarization with KCI and the calcium ionophore ionomycin stimulated nitric oxide synthase (NOS) activity. Characterization of the glutamate response revealed that the ionotropic glutamate receptor agonists N-methyl-D-aspartate (NMDA), kainate and alpha-amino-3-hydroxy-5-methyl-4-isoxalone propionic all stimulated NOS activity with a relative maximal efficacy of NMDA > kainate > alpha-amino-3-hydroxy-5-methyl-4-isoxalone propionic. Ethanol, Mg++ and Zn++ produced a concentration-dependent inhibition of NMDA stimulation of NOS. The Mg++ inhibition was reversed by increasing concentrations of NMDA, whereas Zn++ inhibition was not. Ethanol (100 mM) produced an apparent competitive type inhibition as seen by a parallel right-shift in the NMDA concentration-response curve. However, ethanol inhibition was dependent upon the presence of Mg++ and/or Zn++ in a concentration-related manner. Whereas 100 mM ethanol did not significantly inhibit NMDAstimulation of NOS activity in the absence of Mg++ and Zn++, inclusion of a combination of these cations increased the sensitivity to ethanol such that the NMDA response was completely blocked by 100 mM ethanol IC50 similar to 30 mM). The potency for inhibition of NMDA stimulation of NOS by several short-chain alcohols followed their hydrophobicity profile and showed a similar dependency upon Mg++ for inhibition, alpha-amino-3-hydroxy-5-methy-4-isoxalone propionic, but not kainate, stimulation of NOS was also inhibited by ethanol (100 mM). These resultsindicate that activation of NOS in cultured cerebral cortical neuronsoccurs primarily through ionotropic glutamate receptors that show a differential sensitivity to ethanol inhibition. Ethanol appears to act in an interactive manner with Mg++ and Zn++ ions to inhibit NMDA receptors that couple to stimulation of NOS by potentiating the blocking actions of these cations.

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Documento generato il 02/12/20 alle ore 16:55:27