RATIONALE: Effect of cannabinoid CB1 receptor deletion on cocaine's actions is controversial. This is partly based on findings in CB1-receptor-knockout (CB1(-/-)) mice with CD1 genetic background. OBJECTIVES: In the present study, we used CB1(-/-) mice with a C57BL/6J genetic background to further investigate the role of CB1 receptors in cocaine's action. MATERIALS AND METHODS: Locomotor activity was assessed using AccuScan locomotor chambers. Brain extracellular dopamine (DA) levels were measured by in vivo microdialysis and by fast-scan cyclic voltammetry in the nucleus accumbens (NAc). RESULTS: CB1(-/-) mice displayed a significant reduction in basal levels of locomotion and extracellular DA, as well as in cocaine-enhanced locomotion and extracellular DA, as compared to their wild-type (CB1(+/+)) littermates. The reduction in basal and cocaine-enhanced DA appears to be related to a reduction in basal DA release, not to an increase in DA clearance, as indicated by fast-scan cyclic voltammetry in brain slices. Pharmacological blockade of CB1 receptors by SR141716 inhibited locomotion and NAc DA release in CB1(+/+) mice. CONCLUSIONS: The present findings suggest an important role for CB1 receptors in mediating cocaine's behavioral and neurochemical effects.
RATIONALE: Effect of cannabinoidCB1 receptor deletion on cocaine's actions is controversial. This is partly based on findings in CB1-receptor-knockout (CB1(-/-)) mice with CD1 genetic background. OBJECTIVES: In the present study, we used CB1(-/-) mice with a C57BL/6J genetic background to further investigate the role of CB1 receptors in cocaine's action. MATERIALS AND METHODS: Locomotor activity was assessed using AccuScan locomotor chambers. Brain extracellular dopamine (DA) levels were measured by in vivo microdialysis and by fast-scan cyclic voltammetry in the nucleus accumbens (NAc). RESULTS:CB1(-/-) mice displayed a significant reduction in basal levels of locomotion and extracellular DA, as well as in cocaine-enhanced locomotion and extracellular DA, as compared to their wild-type (CB1(+/+)) littermates. The reduction in basal and cocaine-enhanced DA appears to be related to a reduction in basal DA release, not to an increase in DA clearance, as indicated by fast-scan cyclic voltammetry in brain slices. Pharmacological blockade of CB1 receptors by SR141716 inhibited locomotion and NAc DA release in CB1(+/+) mice. CONCLUSIONS: The present findings suggest an important role for CB1 receptors in mediating cocaine's behavioral and neurochemical effects.
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