Psychology Department, University of Colorado Denver, USA; Current: Department of Biomedical Sciences, Marquette University, USA.
Psychology Department, University of Colorado Denver, USA.
Neuropharmacology. 2021 Jan;182:108374. doi: 10.1016/j.neuropharm.2020.108374. Epub 2020 Oct 25.
Synthetic cannabinoids were introduced into recreational drug culture in 2008 and quickly became one of the most commonly abused drugs in the United States. The neurobiological consequences resulting from synthetic cannabinoid repeated exposure remain poorly understood. It is possible that a blunted dopamine (DA) response may lead drug users to consume larger quantities to compensate for this form of neurochemical tolerance. Because the endogenous cannabinoid and opioid systems exhibit considerable cross-talk and cross-tolerance frequently develops following repeated exposure to either opioids or cannabinoids, there is interest in investigating whether a history of synthetic cannabinoid exposure influences the ability of heroin to increase DA release. To test the effects of chronic cannabinoid exposure on cannabinoid- and heroin-evoked DA release, male adult rats were treated with either vehicle or a synthetic cannabinoid (WIN55-212-2; WIN) using an intravenous (IV) dose escalation regimen (0.2-0.8 mg/kg IV over 9 treatments). As predicted, WIN-treated rats showed a rightward shift in the dose-response relationship across all behavioral/physiological measures when compared to vehicle-treated controls. Then, using fast-scan cyclic voltammetry to measure changes in the frequency of transient DA events in the nucleus accumbens shell of awake and freely-moving rats, it was observed that the DA releasing effects of both WIN and heroin were significantly reduced in male rats with a pharmacological history of cannabinoid exposure. These results demonstrate that repeated exposure to the synthetic cannabinoid WIN can produce tolerance to its DA releasing effects and cross-tolerance to the DA releasing effects of heroin.
合成大麻素于 2008 年引入娱乐性毒品文化,迅速成为美国最常见的滥用药物之一。由于重复暴露于合成大麻素而导致的神经生物学后果仍知之甚少。可能是由于多巴胺(DA)反应迟钝,吸毒者可能会消耗更多的毒品来弥补这种神经化学耐受性。由于内源性大麻素和阿片样物质系统表现出相当大的串扰,并且在反复暴露于阿片样物质或大麻素后经常会产生交叉耐受性,因此人们有兴趣研究合成大麻素暴露史是否会影响海洛因增加 DA 释放的能力。为了测试慢性大麻素暴露对大麻素和海洛因诱发的 DA 释放的影响,雄性成年大鼠用载体或合成大麻素(WIN55-212-2;WIN)进行治疗,使用静脉内(IV)剂量递增方案(0.2-0.8 mg/kg IV 分 9 次给予)。正如预测的那样,与载体处理的对照组相比,WIN 处理的大鼠在所有行为/生理测量中都表现出剂量-反应关系的右移。然后,使用快速扫描循环伏安法测量清醒和自由移动大鼠伏隔核壳中瞬态 DA 事件频率的变化,观察到具有大麻素暴露药理学史的雄性大鼠中,WIN 和海洛因的 DA 释放作用均明显降低。这些结果表明,重复暴露于合成大麻素 WIN 可产生对其 DA 释放作用的耐受性和对海洛因 DA 释放作用的交叉耐受性。