Article Figures & Data
Figures
- Fig. 1.
Effects of the CB1 receptor antagonist on heroin self-administration in Wistar male rats. A, Acute injection of SR 141716A (3 mg/kg) reduced heroin self-administration (0.06 mg/injection) in the next 60 min. B, Time analysis along the 210 min session revealed that the effect of 3 mg/kg SR 141716A was still present 150 min after its administration. At the dose of 0.3 mg/kg, the CB1 antagonist induced a temporary increase in heroin self-administration. The CB1 receptor antagonist failed to modify operant responses for food and did not induce place preference (see Results). *p < 0.01 versus saline-treated group; Newman–Keuls.
- Fig. 2.
Effects of the CB1 receptor antagonist SR 141716A on opiate reinforcement in mice. A, Mice self-administered morphine following a bell-shaped dose–response curve. Injection of morphine or vehicle to active (open bars) and passive (hatched bars) mice was controlled by nose pokes of the active mouse. The number of nose pokes was recorded in n = 6–18 animals per group.B, The CB1 receptor antagonist SR141716A failed to induce self-administration. C, Pretreatment with SR 141716A (0.25 mg/kg, i.p.) 30 min before the onset of the session prevented morphine (2 μg/kg) self-administration. **p < 0.01; *p < 0.05, active versus passive; Newman–Keuls test.
- Fig. 3.
Effects of the administration of the CB1 receptor antagonist SR 141716A in morphine-dependent rats. A,Acute administration of SR 141716A (3 mg/kg) resulted in place aversion as reflected by the significant negative change of preference in morphine-dependent animals. n = 8–12 animals per group; *p < 0.05 SR141716A versus saline treatment; Newman–Keuls. B, CB1 cannabinoid receptor blockade affected operant responding for food (60 min sessions, FR 5, time out 2 min) in food-deprived animals (n = 9), only in morphine-dependent rats. *p < 0.05 SR141716A versus saline treatment; Newman–Keuls.
- Fig. 4.
Acute administration of SR 141716A (3 mg/kg) blocked the expression of an already established morphine-induced place preference in morphine-dependent mice. SL, Saline;MP, morphine, SR, SR141716A. **p < 0.01, morphine-dependent versus saline-treated group; Scheffé F test.
- Fig. 5.
Naloxone administration (1 mg/kg, i.p.) induced a partial cannabinoid withdrawal syndrome in male rats chronically exposed to either the cannabinoid receptor agonist HU-210 (100 μg/kg for 14 d) or to the opiate morphine (2 pellets of 75 mg of morphine base implanted subcutaneously for 72 hr). The cannabinoid antagonist SR 141716A (3 mg/kg) induced a partial cannabinoid withdrawal syndrome in morphine-dependent animals.n = 9–15 animals per group; **p < 0.01; *p < 0.05, versus saline-treated animals; Newman–Keuls test.
- Fig. 6.
Opioid involvement in cannabinoid self-administration. A, Mice did self-inject the CB1 receptor agonist WIN 55,212–2 (50 and 100 μg/kg per injection), although they did not self-inject the opioid receptor antagonist naloxone (NX). However, naloxone (B) (100 μg/kg) decreased the self-administration of the cannabinoid receptor agonists WIN 55,212–2 (WIN; 100 μg/kg per injection) and HU-210 (HU; 100 μg/kg per injection). n = 10–12 animals per group; **p < 0.01, active versus passive; Newman–Keuls test.
- Fig. 7.
Opioid involvement in cannabinoid CB1 receptor mRNA expression in the rat brain, measured by quantitative in situ hybridization histochemistry. A, Acute morphine (5 mg/kg) decreased the expression of the CB1 receptor mRNA in specific brain areas. B, Chronic morphine (2 pellets of 75 mg of morphine base implanted subcutaneously for 72 hr) or opiate withdrawal (removal of morphine pellets for 6 hr) reversed these effects. n = 3–4 animals per group; *p < 0.01, versus vehicle or placebo groups; Newman–Keuls test. CP, Caudate putamen;SPT-ACC, septum shell of accumbens; HDB, horizontal arm of the diagonal band of Broca; VDB, vertical arm of the diagonal band; ACA, anterior amygdaloid nuclei; HBC, habenular complex.
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