Goddard Benjamin, Leri Francesco
Department of Psychology, University of Guelph, Guelph, Ontario, Canada N1G 2W1.
Pharmacol Biochem Behav. 2006 Apr;83(4):540-6. doi: 10.1016/j.pbb.2006.03.015. Epub 2006 May 6.
The aim of the present experiment was to investigate the effects of cocaine primes and exposure to foot shock stress on reinstatement of operant responding maintained by a cocaine-conditioned stimulus in rats never trained to actively self-administer cocaine. Following a baseline session of responding for a light-buzzer compound stimulus, rats underwent classical conditioning whereby the compound stimulus was paired with passive intravenous infusions of cocaine (vehicle, 0.5 or 1.0 mg/kg/inf). On subsequent test sessions, operant responding for the compound stimulus was re-assessed in the absence of cocaine. Finally, rats received a cocaine prime (20 mg/kg, i.p.) and foot shock stress prior to two separate test sessions assessing lever pressing for the cocaine-conditioned stimulus. It was found that the animals conditioned with cocaine displayed sustained responding on the lever activating the cocaine-conditioned stimulus. In addition, priming injections of cocaine reinstated responding for the light-buzzer compound stimulus, and this effect was proportional to the dose of cocaine received during classical conditioning. Foot shock stress also reinstated responding, but its effect was smaller and observed only in animals conditioned with the highest dose of cocaine. These findings suggest that cocaine primes and stress can induce reinstatement by reactivating the motivational value of cocaine-conditioned cues.
本实验的目的是研究可卡因引发剂和足部电击应激对从未接受过主动自我给药可卡因训练的大鼠中由可卡因条件刺激维持的操作性反应恢复的影响。在对光-蜂鸣器复合刺激进行反应的基线期后,大鼠接受经典条件反射,在此过程中,复合刺激与可卡因(溶剂、0.5或1.0毫克/千克/次静脉注射)的被动静脉输注配对。在随后的测试期,在没有可卡因的情况下重新评估对复合刺激的操作性反应。最后,在两次单独的测试期之前,大鼠接受一次可卡因引发剂(20毫克/千克,腹腔注射)和足部电击应激,这两次测试期评估对可卡因条件刺激的杠杆按压。结果发现,用可卡因进行条件反射的动物在激活可卡因条件刺激的杠杆上表现出持续反应。此外,可卡因引发剂注射恢复了对光-蜂鸣器复合刺激的反应,并且这种效应与经典条件反射期间接受的可卡因剂量成比例。足部电击应激也恢复了反应,但其效应较小,且仅在接受最高剂量可卡因条件反射的动物中观察到。这些发现表明,可卡因引发剂和应激可通过重新激活可卡因条件线索的动机价值来诱导反应恢复。