Fig. 3
Optogenetic inhibition of CeA CRF neurons reduced alcohol intake in alcohol-dependent rats. a Timeline of the experiment. b Optogenetic inhibition of CeA CRF neurons did not alter alcohol (a) or water (b) self-administration in nondependent rats. There was no virus × laser treatment interaction (F2,28 = 2.10, p > 0.05, two-way ANOVA). Water self-administration was also unaffected by the green laser, with no virus × laser treatment interaction (F1,28 = 1.07, p > 0.05, two-way ANOVA). c Alcohol self-administration escalated during intermittent alcohol vapor exposure (F1,28 = 0.82, p < 0.001, one-way ANOVA), with intake during sessions 8–12 that was significantly greater than during the first day of vapor exposure (*p < 0.05, Newman Keuls post hoc test). d Effect of optogenetic inhibition of CeA CRF neurons on alcohol (a) and water (b) self-administration. Both control and NpHR-expressing rats escalated their alcohol intake after 5 weeks of vapor exposure (F1,14 = 14.9, p < 0.01; p < 0.05, vs. baseline pre-vapor, Newman Keuls post hoc test). Activation of the green laser selectively reduced escalated alcohol self-administration only in NpHR-expressing rats. There was a significant virus type × laser treatment interaction (F2,28 = 8.38, p < 0.01, two-way ANOVA **p < 0.05, laser ON vs. OFF, after Newman Keuls) for alcohol, but not for water self-administration (F2,28 = 2.44, p > 0.05, two-way ANOVA). e There were no differences in (a) saccharin intake (group × laser treatment interaction: F2,28 = 0.06, p > 0.05, two-way ANOVA) or (b) concomitant water intake (group × laser treatment interaction: F2,28 = 0.27, p > 0.05, two-way ANOVA). f, g Optogenetic inhibition of CeA CRF neurons did not alter the (f) total distance traveled (t8 = 0.36, p > 0.05, paired t-test) or (g) time spent in the center (t8 = 0.36, p > 0.05, paired t-test) in the open field in control rats or NpHR-expressing rats. The data are expressed as mean ± SEM
