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. Author manuscript; available in PMC: 2020 Jan 1.
Published in final edited form as: Neuropharmacology. 2018 Oct 14;144:29–36. doi: 10.1016/j.neuropharm.2018.10.008

Figure 4. Ethanol excitation is attenuated with in vivo downregulation of Kcnk13.

Figure 4.

A, B Ratemeter graphs of the responses to ethanol of single neurons after VTA infection with lentivirus expressing either shScr (A) or shKcnk13 (B). Ethanol (40, 80, 120 mM) produced excitation of (A) 1.85, 26.5, and 37.7 %, and (B) 5.5, 9.9, and 12.8 %.

C. Pooled results from extracellular recordings of VTA neurons in brain slices from mice expressing either shKcnk13 or shScr. The effect of ethanol (40, 80 120 mM) on firing rate was tested. Ethanol excitation was significantly decreased in VTA neurons from shKcnk13 mice compared with control (two-way RM ANOVA, F1, 45= 17.34, p<0.006 for effect of shRNA, n=8). Mean baseline firing between the treatment groups was not significantly different (shScr 1.90 ± 0.46 Hz, shKcnk13, 2.50 ± 0.46 Hz; unpaired t-test, t=1.08, p > 0.05, n=8)