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. Author manuscript; available in PMC: 2011 Feb 1.
Published in final edited form as: Neuropsychopharmacology. 2010 Jun 2;35(9):1984–1996. doi: 10.1038/npp.2010.76

Fig 2. Ethanol increases frequency of spontaneous GoC firing in presence of neurotransmitter receptor antagonists.

Fig 2

A, sample traces illustrating the effect of ethanol on firing. B, timecourse of the 40 mM ethanol-induced Δf (gray circles); the effect of urea (40 mM; white circles) on Δf in presence is also shown, which was tested to determine whether ethanol acted via an osmotic mechanism (n = 13 in all cases). C, plot of the 40 mM ethanol-induced Δf versus basal f. D, dose-response curve for the ethanol-induced Δf (20 mM, n = 10; 40 mM, n = 13; and 80 mM, n = 13; **p < 0.01, ****p < 0.0001 by one-sample t-test vs. zero; ***p < 0.001 by one-way ANOVA followed Bonferroni posthoc test). All results shown in this figure were obtained in the loose-patch cell-attached configuration in presence of gabazine (10 μM), kynurenate (1 mM), D,L-APV (50 μM), strychnine (1 μM), CGP 54626 (10 μM), and LY 341495 (1 μM).