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首页> 外文期刊>Neuron >A Subpopulation of Striatal Neurons Mediates Levodopa-Induced Dyskinesia
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A Subpopulation of Striatal Neurons Mediates Levodopa-Induced Dyskinesia

机译：纹纹神经元的亚群介导左旋多巴诱导的妊肽

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摘要

Parkinson's disease is characterized by the progressive loss of midbrain dopamine neurons. Dopamine replacement therapy with levodopa alleviates parkinsonian motor symptoms but is complicated by the development of involuntary movements, termed levodopa-induced dyskinesia (LID). Aberrant activity in the striatum has been hypothesized to cause LID. Here, to establish a direct link between striatal activity and dyskinesia, we combine optogenetics and a method to manipulate dyskinesia-associated neurons, targeted recombination in active populations (TRAP). We find that TRAPed cells are a stable subset of sensorimotor striatal neurons, predominantly from the direct pathway, and that reactivation of TRAPed striatal neurons causes dyskinesia in the absence of levodopa. Inhibition of TRAPed cells, but not a nonspecific subset of direct pathway neurons, ameliorates LID. These results establish that a distinct subset of striatal neurons is causally involved in LID and indicate that successful therapeutic strategies for treating LID may require targeting functionally selective neuronal subtypes.
机译：帕金森病的特点是中脑多巴胺神经元的进步丧失。多巴胺替代疗法与Levodopa减轻了Parkinsonian电机症状，但由于非自愿运动的发展是复杂的，被称为左旋多巴诱导的腹膜瘤（盖子）。纹状体中的异常活性已被假设引起盖子。在这里，为了建立纹状体活性和止吐肽之间的直接联系，我们将光源和一种操纵止吐剂相关神经元的方法，在活性群体（陷阱）中靶向重组。我们发现捕获的细胞是感官电池纹状体神经元的稳定子集，主要来自直接途径，并且捕获的纹状体神经元的再活化导致止血剂的缺失的左旋多巴。抑制捕获的细胞，但不是直接途径神经元的非特异性子集，改善盖子。这些结果确定纹状体神经元的不同子集是盖子的因因果涉及，并表明治疗盖子的成功治疗策略可能需要靶向功能选择性的神经元亚型。

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