Skip to main content
. Author manuscript; available in PMC: 2018 May 1.
Published in final edited form as: Addict Biol. 2016 Jan 24;22(3):616–628. doi: 10.1111/adb.12353

Figure 3. Adolescent ethanol exposure results in a reduction in the amplitude of the GABAAR tonic current.

Figure 3

A) Representative trace showing tonic GABAAR current, measured as the magnitude of change in holding current after bath application of the GABAAR antagonist picrotoxin (100 μM), in PrL-C slices obtained from control and AIE exposed rats. B) Representative all-point histograms and fitted Gaussian functions for the whole-cell current data showing the peak Ihold before and after picrotoxin in slices from control (left panel) and AIE (middle panel) rats. C) Slices obtained from control rats revealed that the amplitude of the tonic GABAAR current remained stable throughout development and AIE exposure significantly attenuated tonic GABA current at all time-points examined, including shortly after exposure (PD 45 ± 3 days; n = 5-6 cells/group; *p < 0.05), in early adulthood (PD 60 ± 3 days; n = 6-8 cells/group; **p < 0.01), and in the fully mature adult (PD90 ± 6 days; n = 8-10 cells/group; **p < 0.01). D) AIE exposure significantly attenuated tonic GABA current in layer V pyramidal neurons from adult female rats (n = 7-8 cells/group, ***p < 0.001).