Figure 3.

Relative involvement of central vs. peripheral CB1R blockade in the inhibition of voluntary ethanol intake by CB1 antagonists. Mice had access to 20% ethanol for 4 h each day. On day 4, one hour before the dark period, mice were infused intracerebroventricularly (i.c.v.) with (a) rimonabant (2 µg, RIM, R), (b) JD5037 (1 μg, JD) or their solvents (veh, V) and drinking session was repeated one more time. Another cohort of wild-type mice (wt) and/or their CB1 receptor-deficient (Cnr^−/−) counterparts received (c) rimonabant (10 mg/kg), (d) JD5037 (3 mg/kg), or vehicle by oral gavage. Drinking behavior in individual animals is expressed as points before (average of days 1–3) and after treatment (day 4). The corresponding serum ethanol values are shown as mean ± s.e.m. * p < 0.05; *** p < 0.001, compared with before treatment (Student’s t-test for paired samples), ^# p < 0.05 compared with the vehicle (Student’s t-test for unpaired samples), n.s. not significant.