Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden.
Int Rev Neurobiol. 2011;98:95-122. doi: 10.1016/B978-0-12-381328-2.00004-3.
Parkinson's disease (PD), a common neurodegenerative disorder caused by the loss of the dopaminergic input to the basal ganglia, is commonly treated with l-DOPA. Use of this drug, however, is severely limited by the development of dystonic and choreic motor complications, or dyskinesia. This chapter describes the molecular mechanisms implicated in the emergence and manifestation of l-DOPA-induced dyskinesia (LID). Particular emphasis is given to the role played in this condition by abnormalities in signal transduction at the level of the medium spiny neurons (MSNs) of the striatum, which are the principal target of l-DOPA. Recent evidence pointing to pre-synaptic dysregulation is also discussed.
帕金森病（PD）是一种常见的神经退行性疾病，由基底神经节中多巴胺能输入的丧失引起，通常用 l-DOPA 治疗。然而，这种药物的使用受到严重限制，因为它会引起张力障碍和舞蹈样运动并发症，或运动障碍。本章描述了与 l-DOPA 诱导的运动障碍（LID）的出现和表现有关的分子机制。特别强调了在纹状体中间神经元（MSNs）水平的信号转导异常在这种情况下所起的作用，MSNs 是 l-DOPA 的主要靶标。还讨论了最近指向突触前失调的证据。
