Neuropeptide modulation of central amygdala neuroplasticity is a key mediator of alcohol dependence

NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS

卷:36

Review

Gilpin, Nicholas W.¹  Roberto, Marisa² 

[1] Louisiana State Univ, Hlth Sci Ctr, Dept Physiol, New Orleans, LA 70112 USA

[2] Scripps Res Inst, Comm Neurobiol Addict Disorders, La Jolla, CA 92037 USA

关键词: Central amygdala;    GABA;    Glutamate;    CRF;    NPY;    Nociceptin;    Dynorphin;    Galanin;    Cannabinoids;    Neuropeptides;    Alcohol dependence;   

DOI  :  10.1016/j.neubiorev.2011.11.002

来源: Elsevier

【 摘 要 】

Alcohol use disorders are characterized by compulsive drug-seeking and drug-taking, loss of control in limiting intake, and withdrawal syndrome in the absence of drug. The central amygdala (CeA) and neighboring regions (extended amygdala) mediate alcohol-related behaviors and chronic alcohol-induced plasticity. Acute alcohol suppresses excitatory (glutamatergic) transmission whereas chronic alcohol enhances glutamatergic transmission in CeA. Acute alcohol facilitates inhibitory (GABAergic) transmission in CeA, and chronic alcohol increases GABAergic transmission. Electrophysiology techniques are used to explore the effects of neuropeptides/neuromodulators (CRF, NPY, nociceptin, dynorphin, endocannabinoids, galanin) on inhibitory transmission in CeA. In general, pro-anxiety peptides increase, and anti-anxiety peptides decrease CeA GABAergic transmission. These neuropeptides facilitate or block the action of acute alcohol in CeA, and chronic alcohol produces plasticity in neuropeptide systems, possibly reflecting recruitment of negative reinforcement mechanisms during the transition to alcohol dependence. A disinhibition model of CeA output is discussed in the context of alcohol dependence- and anxiety-related behaviors. (c) 2011 Elsevier Ltd. All rights reserved.

【 授权许可】

Free