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. Author manuscript; available in PMC: 2017 Oct 19.
Published in final edited form as: Neuron. 2016 Oct 6;92(2):493–504. doi: 10.1016/j.neuron.2016.09.029

Figure 8. KCC2 activation in the VTA prevents stress-ethanol interaction.

Figure 8

A) When brain slices were incubated in the KCC2 activator, CLP290, EGABA was hyperpolarized comparably in VTA GABA neurons from control (black) and stressed (red) animals. The effect of stress exposure on EGABA in the absence of CLP290 is shown for comparison (open red square), n = 6 cells/group

B) After CLP290 incubation, ethanol-induced VTA DA neuron firing was no longer attenuated after exposure to stress (red) and was similar to the response of the unstressed controls (black). The effect of stress exposure and ethanol application in the absence of CLP290 is shown for comparison (dotted red line), n = 10 cells/group. Note, incubation of VTA slices with CLP290 (before ethanol) did not produce any significant alterations in the mean basal firing rate of DA neurons between control and stress groups.

C) CLP290 was infused bilaterally intra-VTA (40 µM at 0.5 µl/min). After CLP290 administration, stressed animals consumed significantly less ethanol (blue) compared to vehicle-injected stressed animals (red). Ethanol consumption in unstressed control rats is shown for comparison (dotted horizontal line). *Significantly different from the VTA vehicle group by t-test, p < 0.05, n = 12–13 rats/group.