期刊
TRENDS IN NEUROSCIENCES
卷 35, 期 10, 页码 587-596出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tins.2012.05.005
关键词
addiction; dynorphin; kappa-opioid receptor; heroin; prescription opioids; cocaine
资金
- National Institutes of Health, National Institute on Drug Abuse [P60 DA05130]
- National Institute of Mental Health grant [MH70880]
- National Center for Research Resources (Center for Clinical and Translational Science) [UL1RR024143]
Addictions to cocaine or heroin/prescription opioids [short-acting mu-opioid receptor (MOPr) agonists] involve relapsing cycles, with experimentation/escalating use, withdrawal/abstinence, and relapse/re-escalation. kappa-Opioid receptors (KOPr; encoded by OPRK1), and their endogenous agonists, the dynorphins (encoded by PDYN), have counter-modulatory effects on reward caused by cocaine or MOPr agonist exposure, and exhibit plasticity in addictive-like states. KOPr/dynorphin activation is implicated in depression/anxiety, often comorbid with addictions. In this opinion article we propose that particular stages of the addiction cycle are differentially affected by KOPr/dynorphin systems. Vulnerability and resilience can be due to pre-existing (e.g., genetic) factors, or epigenetic modifications of the OPRK1 or PDYN genes during the addiction cycle. Pharmacotherapeutic approaches limiting changes in KOPr/dynorphin tone, especially with KOPr partial agonists, may hold potential for the treatment of specific drug addictions and psychiatric comorbidity.
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