Neuroscience Graduate Group, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, United States of America; Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, United States of America.
Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, United States of America; Department of Biobehavioral Health Sciences, School of Nursing, University of Pennsylvania, Philadelphia, PA 19104, United States of America.
Physiol Behav. 2019 Jul 1;206:93-105. doi: 10.1016/j.physbeh.2019.03.026. Epub 2019 Mar 28.
Given that the search for effective pharmacotherapies for cocaine use disorder has, thus far, been fruitless, there remains a critical need for conceptually innovative approaches toward identifying new medications to treat this disease. A better understanding of the neurocircuits and neurobiological mechanisms underlying cocaine taking and seeking may identify molecular substrates that could serve as targets for novel pharmacotherapies to treat cocaine use disorder. Recent preclinical evidence suggests that glucagon-like peptide-1 (GLP-1) receptor agonists could be re-purposed to treat cocaine craving-induced relapse. This review endeavors to comprehensively summarize the current literature investigating the efficacy of GLP-1 receptor agonists in reducing the rewarding and reinforcing effects of cocaine in animal models of cocaine use disorder. The role of central endogenous GLP-1 circuits in voluntary cocaine taking and seeking is also discussed. Behavioral, neurochemical, electrophysiological and molecular biology studies indicate that central GLP-1 receptor activation functionally modulates the mesolimbic reward system and decreases addiction-like phenotypes in rodents. Overall, an emerging preclinical literature provides compelling evidence to advance GLP-1 receptor agonists into clinical trials testing the efficacy of these medications in preventing cocaine craving-induced relapse.
鉴于迄今为止,寻找可卡因使用障碍的有效药物治疗方法尚未取得成果,因此仍然迫切需要从概念上创新的方法来确定治疗这种疾病的新药。更好地了解可卡因摄入和寻求的神经回路和神经生物学机制,可以确定可能成为治疗可卡因使用障碍的新型药物治疗靶点的分子底物。最近的临床前证据表明,胰高血糖素样肽-1(GLP-1)受体激动剂可以重新用于治疗可卡因渴望引起的复发。这篇综述旨在全面总结当前研究 GLP-1 受体激动剂在减少可卡因使用障碍动物模型中可卡因奖赏和强化作用的疗效的文献。还讨论了中枢内源性 GLP-1 回路在自愿性可卡因摄入和寻求中的作用。行为、神经化学、电生理学和分子生物学研究表明,中枢 GLP-1 受体的激活可调节中脑边缘奖赏系统的功能,并减少啮齿动物的成瘾样表型。总的来说,新兴的临床前文献提供了令人信服的证据,将 GLP-1 受体激动剂推进临床试验,以测试这些药物预防可卡因渴望引起的复发的疗效。