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. 2013 Oct 8;3(10):e310. doi: 10.1038/tp.2013.72

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Copyright © 2013 Macmillan Publishers Limited

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/

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The nor-BNI (nBNI) pretreatment reverses the effects of ethanol on the basal- and potassium-induced dialysate concentrations of glutamate in the CA3 area of the hippocampus. (a) The time pattern of the basal- and potassium-stimulated extracellular glutamate concentration in the CA3 area of the hippocampus of the water- and ethanol-treated rats. The left panel shows the effects of vehicle (n=6) or nor-BNI (n=4) treatment on the water-exposed rats, and the right panel shows the effects of vehicle (n=7) or nor-BNI (n=7) treatment on the ethanol-exposed rats. The nor-BNI treatment normalized the glutamate concentrations in the ethanol-exposed rats but failed to influence those of the water-exposed rats. (b) The bar graphs of the area under the curve (AUC) values for the stimulated glutamate levels. *P⩽0.05; the significance of the differences between the water-vehicle and ethanol-vehicle treatment group; and between the ethanol-nor-BNI and ethanol-vehicle treatment group.