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影响海马体突触可塑性的烟碱机制。

Nicotinic mechanisms influencing synaptic plasticity in the hippocampus.

作者信息

Placzek Andon Nicholas, Zhang Tao A, Dani John Anthony

机构信息

Department of Neuroscience, Baylor College of Medicine, Houston, TX 77030, USA.

出版信息

Acta Pharmacol Sin. 2009 Jun;30(6):752-60. doi: 10.1038/aps.2009.39. Epub 2009 May 11.

Abstract

Nicotinic acetylcholine receptors (nAChRs) are expressed throughout the hippocampus, and nicotinic signaling plays an important role in neuronal function. In the context of learning and memory related behaviors associated with hippocampal function, a potentially significant feature of nAChR activity is the impact it has on synaptic plasticity. Synaptic plasticity in hippocampal neurons has long been considered a contributing cellular mechanism of learning and memory. These same kinds of cellular mechanisms are a factor in the development of nicotine addiction. Nicotinic signaling has been demonstrated by in vitro studies to affect synaptic plasticity in hippocampal neurons via multiple steps, and the signaling has also been shown to evoke synaptic plasticity in vivo. This review focuses on the nAChRs subtypes that contribute to hippocampal synaptic plasticity at the cellular and circuit level. It also considers nicotinic influences over long-term changes in the hippocampus that may contribute to addiction.

摘要

烟碱型乙酰胆碱受体(nAChRs)在整个海马体中均有表达,烟碱信号传导在神经元功能中起着重要作用。在与海马体功能相关的学习和记忆相关行为的背景下,nAChR活性的一个潜在重要特征是它对突触可塑性的影响。海马体神经元中的突触可塑性长期以来一直被认为是学习和记忆的一种细胞机制。同样类型的细胞机制也是尼古丁成瘾发展的一个因素。体外研究表明,烟碱信号传导通过多个步骤影响海马体神经元的突触可塑性,并且该信号传导在体内也能诱发突触可塑性。本综述聚焦于在细胞和回路水平上对海马体突触可塑性有贡献的nAChR亚型。它还考虑了烟碱对海马体中可能导致成瘾的长期变化的影响。

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