Article Figures & Data
Figures
- Figure 1.
Endocannabinoids mediate cocaine-induced increases in subsecond dopamine release. A, Representative traces of dopamine extracellular concentration fluctuations after an injection of cocaine after saline (top), the attenuation of this response by rimonabant after a second cocaine administration (middle) in the same animal and recording location, as well as the effects of saline injection at the same site (bottom). The arrow and dashed line indicate time of drug administration. B, Pooled data of the frequency of dopamine transients (fDA) in the 4.5 min after the end of each intravenous drug infusion (animals in the control group are shown in white bars). S, Saline; C, first dose of cocaine (3 mg/kg); V/Ri, vehicle (n = 4) or rimonabant (n = 5; 0.3 mg/kg) injection 4.5 min after first dose of cocaine; C2, second dose of cocaine (3 mg/kg) given 30 min after vehicle or rimonabant (Scheffé's test, *p < 0.05 compared with saline; Bonferroni's test, ∧ p < 0.05 vehicle vs rimonabant-treated animals; Bonferroni's test, &p < 0.05 vehicle vs rimonabant-treated animals). C, Amplitude of drug-evoked dopamine transients ([DA]max). Error bars indicate SEM.
- Figure 2.
Cannabinoid receptor blockade attenuates the effects of ethanol of subsecond dopamine release. A, Traces depicting ethanol-induced extracellular dopamine fluctuations after saline injection (top), the attenuation of this response by rimonabant after the second ethanol administration (middle) in the same animal and recording location, and the effects of saline injection at the same site (bottom). The arrow and dashed line indicate time of drug administration. B, Pooled data from ethanol-responsive sites of the frequency of dopamine transients (fDA) in the 4.5 min after the end of each intravenous drug infusion (animals in the control group are shown in white bars). S, Saline; E, first dose of ethanol (1 g/kg); V/Ri, vehicle (n = 8) or rimonabant (n = 9; 0.3 mg/kg) injection 4.5 min after first dose of ethanol; E2, second dose of ethanol (1 g/kg) given 30 min after vehicle or rimonabant (Scheffé's test, *p < 0.05 compared with saline). C, Amplitude of drug-evoked dopamine transients ([DA]max). Error bars indicate SEM.
- Figure 3.
Nicotine elicits a potent dopamine spillover mediated by CB1 receptors. A, Dopamine trace showing the effects of nicotine injected after saline on subsecond dopamine release (top) and the dopamine response to nicotine when injected to a different animal in the presence of rimonabant (middle). The bottom panel shows the effects of vehicle injection (recorded from the same site as the trace shown in the top panel). The arrow and dashed line indicate time of drug administration. B, Pooled data of the frequency of dopamine transients (fDA) in the 4.5 min after the end of each intravenous drug infusion. V/Ri, Vehicle (n = 4) or rimonabant (n = 4; 0.3 mg/kg) injection; nicotine injection (0.3 mg/kg) given 4.5 min after vehicle (V-nic) or rimonabant (Ri-nic). (Student's t test, *p < 0.05 compared with vehicle; &p < 0.05, vehicle vs rimonabant-treated animals). C, Amplitude of drug-evoked dopamine transients ([DA]max). Error bars indicate SEM.
Additional Files
Supplemental Data
Files in this Data Supplement:
- supplemental material - Figure legends
- supplemental material - Figure 1
- supplemental material - Figure 2
