Figure 3.

Endocannabinoids are necessary for drug-induced increases in tonic and phasic dopamine release. (A) Endocannabinoids are required for ethanol-induced increases in tonic dopamine concentrations in the nucleus accumbens. When administered independently, ethanol (1.5 g/kg, filled squares) increased dopamine concentrations. When coadministered with rimonabant (3 mg/kg i.p., open triangles), ethanol failed to increase accumbal dopamine concentrations. (Figure constructed from data by Hungund et al. 2003.) (B) Disrupting endocannabinoid signaling with rimonabant (1 mg/kg i.v., bottom) reversed ethanol-induced (0.5 g/kg i.v., top) increases in the neural activity of an antidromically identified ventral tegmental area dopamine neuron. (Figure constructed from data by Perra et al. 2005.) (C) Endocannabinoids are required for drug-induced phasic dopamine events. Cocaine (3 mg/kg i.v., top) significantly increased transient increases in nucleus accumbens dopamine concentration. Rimonabant coadministration (0.3 mg/kg i.v., middle) significantly attenuated the cocaine-induced increases in phasic dopamine release. Vehicle alone failed to alter phasic dopamine events (bottom). (Figure constructed from data by Cheer et al. 2007.)