Neuropeptide modulation of central amygdala neuroplasticity is a key mediator of alcohol dependence.
Neuropeptide modulation of central amygdala neuroplasticity is a key mediator of alcohol dependence.
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DOI：
10.1016/j.neubiorev.2011.11.002
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发表时间：
2012-02
影响因子：
8.2
通讯作者：
Roberto, Marisa
中科院分区：
文献类型：
--
作者：
Gilpin, Nicholas W.;Roberto, Marisa
关键词：
酒精使用障碍的特征是强迫性寻求药物和吸毒、限制摄入量失控以及在没有药物的情况下出现戒断综合征。中央杏仁核（CeA）和邻近区域（扩展杏仁核）介导与酒精相关的行为和慢性酒精引起的可塑性。急性酒精抑制兴奋性（谷氨酸）传递，而慢性酒精则增强 CeA 中的谷氨酸传递。急性酒精促进 CeA 中的抑制性（GABA 能）传递，而慢性酒精则增加 GABA 能传递。电生理学技术用于探索神经肽/神经调节剂（CRF、NPY、痛敏肽、强啡肽、内源性大麻素、甘丙肽）对 CeA 抑制性传导的影响。一般来说，促焦虑肽增加，抗焦虑肽减少 CeA GABA 能传递。这些神经肽促进或阻止急性酒精在 CeA 中的作用，而慢性酒精在神经肽系统中产生可塑性，可能反映了在向酒精依赖过渡期间负强化机制的招募。在酒精依赖和焦虑相关行为的背景下讨论了 CeA 输出的去抑制模型。
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.
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