Pan Jing, Cai Huaibin
Transgenics Section, Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Building 35, Room 1A112, MSC 3707, 35 Convent Drive, Bethesda, MD 20892-3707 USA.
Transl Neurodegener. 2017 Jan 17;6:1. doi: 10.1186/s40035-017-0071-y. eCollection 2017.
L-3, 4-Dihydroxyphenylalanine (L-DOPA)-induced dyskinesia (LID) is a major clinical complication in the treatment of Parkinson's disease (PD). This debilitating side effect likely reflects aberrant compensatory responses for a combination of dopaminergic neuron denervation and repeated L-DOPA administration. Abnormal endogenous opioid signal transduction pathways in basal ganglia have been well documented in LID. Opioid receptors have been targeted to alleviate the dyskinesia. However, the exact role of this altered opioid activity is remains under active investigation. In the present review, we discuss the current understanding of opioid signal transduction in the basal ganglia and how the malfunction of opioid signaling contributes to the pathophysiology of LID. Further study of the opioid system in LID may lead to new therapeutic targets and improved treatment of PD patients.
左旋3,4-二羟基苯丙氨酸（L-多巴）诱发的异动症（LID）是帕金森病（PD）治疗中的主要临床并发症。这种使人衰弱的副作用可能反映了多巴胺能神经元去神经支配和反复给予L-多巴共同作用下的异常代偿反应。在LID中，基底神经节内异常的内源性阿片信号转导通路已有充分记录。阿片受体已成为减轻异动症的靶点。然而，这种改变的阿片活性的确切作用仍在积极研究中。在本综述中，我们讨论了目前对基底神经节中阿片信号转导的理解，以及阿片信号传导功能障碍如何导致LID的病理生理学。对LID中阿片系统的进一步研究可能会带来新的治疗靶点，并改善PD患者的治疗。
