神经肽对中枢杏仁核神经可塑性的调节是酒精依赖的关键介质。
Neuropeptide modulation of central amygdala neuroplasticity is a key mediator of alcohol dependence.
机构信息
Department of Physiology, Louisiana State University Health Sciences Center, 1901 Perdido Street, New Orleans, LA 70112, USA.
出版信息
Neurosci Biobehav Rev. 2012 Feb;36(2):873-88. doi: 10.1016/j.neubiorev.2011.11.002. Epub 2011 Nov 11.
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.
酒精使用障碍的特征是强迫性觅药和用药、限制摄入的失控以及停药后的戒断综合征。中央杏仁核（CeA）及其相邻区域（扩展杏仁核）介导与酒精相关的行为和慢性酒精诱导的可塑性。急性酒精抑制兴奋性（谷氨酸能）传递，而慢性酒精增强 CeA 中的谷氨酸能传递。急性酒精促进 CeA 中的抑制性（GABA 能）传递，而慢性酒精增加 GABA 能传递。电生理学技术用于探索神经肽/神经调质（CRF、NPY、孤啡肽、强啡肽、内源性大麻素、甘丙肽）对 CeA 抑制性传递的影响。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断急性酒精在 CeA 中的作用，慢性酒精会使神经肽系统产生可塑性，这可能反映了在向酒精依赖过渡过程中招募了负强化机制。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。
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