Alcohol dependence is a chronically relapsing disorder characterized by compulsive drug-seeking and drug-taking, loss of control in limiting intake, and the emergence of a withdrawal syndrome in the absence of the drug. Accumulating evidence suggests an important role for synaptic transmission in the central nucleus of the amygdala (CeA) in mediating alcohol-related behaviors and neuroadaptive mechanisms associated with alcohol dependence. Acute alcohol facilitates γ-aminobutyric acid (GABA)ergic transmission in the CeA via both pre- and postsynaptic mechanisms, and chronic alcohol increases baseline GABAergic transmission. Acute alcohol inhibits glutamatergic transmission via effects at N-methyl-d-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in the CeA, whereas chronic alcohol up-regulates NMDA receptor (NMDAR)-mediated transmission. Pro- (e.g., corticotropin-releasing factor [CRF]) and antistress (e.g., nociceptin/orphanin FQ, oxytocin) neuropeptides affect alcohol- and anxiety-related behaviors, and also alter the alcohol-induced effects on CeA neurotransmission. Alcohol dependence produces plasticity in these neuropeptide systems, reflecting a recruitment of those systems during the transition to alcohol dependence.

中文翻译：

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中央杏仁核在酒精依赖中的作用

酒精依赖是一种慢性复发性疾病，其特征在于强迫性寻求药物和服用药物，失去限制摄入量的控制以及在没有药物的情况下出现戒断综合征。越来越多的证据表明，突触传递在杏仁核（CeA）的中央核中在介导酒精相关行为和与酒精依赖相关的神经适应机制中起着重要作用。急性酒精通过突触前和突触后机制促进CeA中的γ-氨基丁酸（GABA）能量传递，而慢性酒精会增加基线GABA能量传递。急性酒精通过影响N-甲基-d抑制谷氨酸能传递-CeA中的天冬氨酸（NMDA）和α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）受体，而慢性酒精则上调NMDA受体（NMDAR）介导的传递。前肽（例如，促肾上腺皮质激素释放因子[CRF]）和抗应激（例如，伤害感受器/孤儿蛋白FQ，催产素）神经肽会影响与酒精和焦虑相关的行为，并且还会改变酒精对CeA神经传递的诱导作用。酒精依赖性在这些神经肽系统中产生可塑性，反映出在向酒精依赖性过渡期间这些系统的募集。