Guercio Leonardo A, Schmidt Heath D, Pierce R Christopher
Neuroscience Graduate Group, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA; Center for Neurobiology and Behavior, Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, 125 S. 31st Street, Philadelphia, PA 19104, USA.
Center for Neurobiology and Behavior, Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, 125 S. 31st Street, Philadelphia, PA 19104, USA.
Behav Brain Res. 2015 Mar 15;281:125-30. doi: 10.1016/j.bbr.2014.12.025. Epub 2014 Dec 18.
Stimuli previously associated with drug taking can become triggers that can elicit craving and lead to relapse of drug-seeking behavior. Here, we examined the influence of deep brain stimulation (DBS) in the nucleus accumbens shell on cue-induced reinstatement of cocaine seeking, an animal model of relapse. Rats were allowed to self-administer cocaine (0.254 mg, i.v.) for 2 h daily for 21 days, with each infusion of cocaine being paired with a cue light. After 21 days of self-administration, cocaine-taking behavior was extinguished by replacing cocaine with saline in the absence of the cue light. Next, during the reinstatement phase, DBS was administered bilaterally into the nucleus accumbens shell through bipolar stainless steel electrodes immediately prior to re-exposure to cues previously associated with cocaine reinforcement. DBS continued throughout the 2 h reinstatement session. Parallel studies examined the influence of accumbens shell DBS on reinstatement induced by cues previously associated with sucrose reinforcement. Results indicated that DBS of the nucleus accumbens shell significantly attenuated cue-induced reinstatement of cocaine and sucrose seeking. Together, these results indicate that DBS of the accumbens shell disrupts cue-induced reinstatement associated with both a drug and a natural reinforcer.
先前与药物摄取相关的刺激可成为引发渴望并导致觅药行为复发的触发因素。在此，我们研究了伏隔核壳内深部脑刺激（DBS）对线索诱导的可卡因觅求恢复的影响，这是一种复发的动物模型。大鼠每天被允许静脉注射可卡因（0.254毫克）2小时，持续21天，每次注射可卡因时伴有提示灯。在自我给药21天后，在无提示灯的情况下用生理盐水替代可卡因，从而消除可卡因摄取行为。接下来，在恢复阶段，在重新暴露于先前与可卡因强化相关的线索之前，通过双极不锈钢电极将DBS双侧施加到伏隔核壳内。DBS在整个2小时的恢复过程中持续进行。平行研究考察了伏隔核壳DBS对先前与蔗糖强化相关的线索诱导的恢复的影响。结果表明，伏隔核壳的DBS显著减弱了线索诱导的可卡因和蔗糖觅求的恢复。总之，这些结果表明，伏隔核壳的DBS破坏了与药物和天然强化物相关的线索诱导的恢复。
