Pisani Antonio, Bernardi Giorgio, Ding Jun, Surmeier D James
Fondazione Santa Lucia IRCCS, and Clinica Neurologica, Dipartimento di Neuroscienze, Università di Roma Tor Vergata, Via Montpellier 1, 00135, Rome, Italy.
Trends Neurosci. 2007 Oct;30(10):545-53. doi: 10.1016/j.tins.2007.07.008. Epub 2007 Sep 29.
Twenty years ago, striatal cholinergic neurons were central figures in models of basal ganglia function. But since then, they have receded in importance. Recent studies are likely to lead to their re-emergence in our thinking. Cholinergic interneurons have been implicated as key players in the induction of synaptic plasticity and motor learning, as well as in motor dysfunction. In Parkinson's disease and dystonia, diminished striatal dopaminergic signalling leads to increased release of acetylcholine by interneurons, distorting network function and inducing structural changes that undoubtedly contribute to the symptoms. By contrast, in Huntington's disease and progressive supranuclear palsy, there is a fall in striatal cholinergic markers. This review gives an overview of these recent experimental and clinical studies, placing them within the context of the pathogenesis of movement disorders.
二十年前，纹状体胆碱能神经元是基底神经节功能模型中的核心角色。但从那时起，它们的重要性逐渐降低。最近的研究可能会使它们在我们的认知中重新凸显。胆碱能中间神经元被认为是诱导突触可塑性和运动学习以及运动功能障碍的关键因素。在帕金森病和肌张力障碍中，纹状体多巴胺能信号减弱导致中间神经元释放乙酰胆碱增加，从而扭曲网络功能并引发结构变化，这些变化无疑会导致症状出现。相比之下，在亨廷顿舞蹈症和进行性核上性麻痹中，纹状体胆碱能标志物会减少。本综述概述了这些最新的实验和临床研究，并将它们置于运动障碍发病机制的背景下。
