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Titolo:
Direct evidence for a cause-effect link between ethanol potentiation of GABA(A) receptor function and intoxication from hyperbaric studies in C57, LS, and SS mice
Autore:
Davies, DL; Alkana, RL;
Indirizzi:
Univ So Calif, Sch Pharm, Dept Mol Pharmacol & Toxicol, Alcohol & Brain Res Lab, Los Angeles, CA 90033 USA Univ So Calif Los Angeles CA USA 90033 Res Lab, Los Angeles, CA 90033 USA
Titolo Testata:
ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
fascicolo: 8, volume: 25, anno: 2001,
pagine: 1098 - 1106
SICI:
0145-6008(200108)25:8<1098:DEFACL>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
GAMMA-AMINOBUTYRIC-ACID; SHORT-SLEEP MICE; PRESSURE REVERSAL; CHLORIDE CHANNELS; ION CHANNELS; GENERAL-ANESTHESIA; GLYCINE RECEPTORS; C57BL/6J MICE; LONG-SLEEP; ALCOHOL;
Keywords:
hyperbaric exposure; direct ethanol antagonist; GABA(A) receptors; mouse microsacs;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
58
Recensione:
Indirizzi per estratti:
Indirizzo: Davies, DL Univ So Calif, Sch Pharm, Dept Mol Pharmacol & Toxicol, Alcohol& Brain Res Lab, Los Angeles, CA 90033 USA Univ So Calif Los Angeles CA USA 90033 s Angeles, CA 90033 USA
Citazione:
D.L. Davies e R.L. Alkana, "Direct evidence for a cause-effect link between ethanol potentiation of GABA(A) receptor function and intoxication from hyperbaric studies in C57, LS, and SS mice", ALC CLIN EX, 25(8), 2001, pp. 1098-1106

Abstract

Background: This article uses a direct ethanol antagonist, increased atmospheric pressure, to further test the causative link between ethanol potentiation of gamma -aminobutyric acid (GABA) type A receptor function and ethanol's behavioral effects. This was done by determining whether initial biochemical findings in Iona-sleep (LS) mice extended to other genotypes and whether the previously reported insensitivity of short-sleep (SS) mice to pressure antagonism of ethanol-induced loss of righting reflex extended to a nonselected ethanol-induced behavior. Methods: The effects of 12 times normal atmospheric pressure of helium-oxygen gas (heliox) versus ethanol (25-200 mM) potentiation of GABA-activated Cl- uptake in brain membranes (microsacs) from C57 LS, and SS mice were tested by using a Cl-36(-) flux assay. The effects of pressure versus ethanol's (2 g/kg) anticonvulsant effect in SS mice were tested by using time to onset of isoniazid-induced myoclonic seizures. Results: Exposure to 12 times normal atmospheric pressure heliox antagonized ethanol potentiation of GABA-activated Cl- uptake in all three genotypesacross a range of ethanol concentrations that cause ethanol's behavioral and anesthetic effects. Pressure did not affect baseline receptor function. The threshold for initiating ethanol potentiation differed between genotypes in accordance with their behavioral sensitivities to ethanol (C57 and LS,less than or equal to 25 mM; SS, > 50 mM.). Pressure antagonized ethanol'santiconvulsant effect in SS mice. Conclusions: The results add important direct evidence supporting the hypothesis that ethanol potentiation of GABA, receptor function is an initial action of ethanol causing its behavioral effects. These findings also provide insight into possible effects of selective breeding on GABAA receptor function.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 19:41:33