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  • Title: Chronic ethanol consumption alters recovery of spontaneously active medial septal/diagonal band of broca neurons from GABA-microiontophoresis.
    Author: Matthews DB, Criswell HE, Grobin AC, Morrow AL.
    Journal: Alcohol Clin Exp Res; 2000 Sep; 24(9):1427-32. PubMed ID: 11003210.
    Abstract:
    BACKGROUND: Acute ethanol administration increases GABA-mediated inhibition in a variety of cerebral cortical preparations. Furthermore, chronic ethanol administration blunts ethanol-induced increases in GABA-mediated inhibition and alters GABA A receptor subunit mRNA and peptide expression in the cerebral cortex. The sedative hypnotic effects of ethanol are believed to be modulated by GABA-induced inhibition in medial septum/diagonal band of Broca (MS/DB) neurons, a brain region where acute ethanol administration increases GABA-mediated inhibition of spontaneously active neurons. Chronic ethanol administration produces tolerance to the sedative effects of ethanol. However, it is unknown if chronic ethanol consumption produces alterations in GABA-mediated inhibition in the MS/DB in a manner similar to that found in the cerebral cortex. METHODS: Animals either consumed ethanol chronically for 14 days via a liquid diet or were pair-fed an equicaloric dextrose-containing control diet. Spontaneously active MS/DB neurons were recorded using multibarrel glass micropipettes while the effect of GABA-microiontophoresis was investigated. The total amount of GABA-mediated inhibition at four ejection currents was analyzed, as was the recovery to spontaneous neural firing rates following GABA inhibition. In a separate group of animals, the medial septum was microdissected, and the relative expression of GABA A receptor alpha1 and alpha4 subunit peptide were analyzed via Western blot analysis. RESULTS: Chronic ethanol consumption altered recovery of spontaneous neural activity of MS/DB neurons following GABA-microiontophoresis compared to premicroiontophoresis levels. Specifically, the recovery of spontaneous neural activity of MS/DB neurons recorded from animals that chronically consumed ethanol was slower following GABA-microiontophoresis compared to neurons recorded from control animals. This effect was temporary and reversible. Furthermore, the alteration in recovery of spontaneous neural activity was not due to changes in the total amount of inhibition produced by GABA. Finally, there was no significant change in GABA A receptor alpha1 and alpha4 subunit peptide levels in the MS/DB. CONCLUSIONS: Chronic ethanol consumption alters the frequency of spontaneous MS/DB neural activity following GABA microiontophoresis compared to premicroiontophoresis levels. These data suggest that the kinetics of GABA A receptors in the MS/DB are altered by chronic ethanol consumption independent of changes in the total amount of inhibition or alterations in GABA A receptor alpha1 and alpha4 subunit peptide expression.
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