作者: Miguel Luj n , Laia Alegre Zurano , Ana Mart n S nchez , Olga Valverde
DOI: 10.22541/AU.158987187.70882703
关键词: Facilitation 、 Pharmacology 、 Ventral striatum 、 Prefrontal cortex 、 Cannabidiol 、 AMPA receptor 、 Medicine 、 Extinction (psychology) 、 Cannabinoid receptor 、 Antagonist
摘要: BACKGROUND AND PURPOSE: Pharmacological treatments are unavailable to patients with cocaine use disorders. Efforts develop pharmacotherapies have led the study of cannabidiol, a constituent C. sativa plant. However, specific effects and mechanisms action cannabidiol in rodent model extinction-based abstinence drug seeking relapse remain unclear. EXPERIMENTAL APPROACH: In this study, was provided during extinction training male CD-1 mice trained self-administer cocaine. We evaluated reinstatement induced by cues, stress, priming. To ascertain participation CB1 receptors these behavioural changes, we administered neutral antagonist AM4113 before each session. KEY RESULTS The results document that did not modulate learning. After treatment, increased levels receptor protein were found prelimbic orbitofrontal parts prefrontal cortex, as well ventral striatum; an effect paralleled reduction ∆FosB accumulation GluR2 AMPA subunits. Furthermore, cue-induced prevented cannabidiol-treated mice. Unexpectedly, facilitated stress-induced cocaine-maintained responding. Cocaine-primed remained unaltered cannabidiol. Both, blockade facilitation abolished CONCLUSION IMPLICATIONS: Our reveal series complex CB1-related changes opposite implications for behaviour may limit therapeutic opportunities.