Perez Xiomara A, Zhang Danhui, Bordia Tanuja, Quik Maryka
Bioscience Division, SRI International, Menlo Park, California, USA.
Mov Disord. 2017 Apr;32(4):538-548. doi: 10.1002/mds.26955. Epub 2017 Mar 3.
Dyskinesias are a disabling motor complication that arises with prolonged l-dopa treatment. Studies using D1 receptor drugs and genetically modified mice suggest that medium spiny neurons expressing D1 receptors play a primary role in l-dopa-induced dyskinesias. However, the specific role of these neurons in dyskinesias is not fully understood.
We used optogenetics, which allows for precise modulation of select neurons in vivo, to investigate whether striatal D1-expressing medium spiny neuron activity regulates abnormal involuntary movements or dyskinesia in parkinsonian mice. D1-cre mice unilaterally lesioned with 6-hydroxydopamine received striatal injections of cre-dependent channelrhodopsin2 virus or control virus. After stable virus expression, the effect of optical stimulation on dyskinesia was tested in l-dopa-naïve and l-dopa-primed mice.
Single-pulse and burst-optical stimulation of D1-expressing medium spiny neurons induced dyskinesias in l-dopa-naïve channelrhodopsin2 mice. In stably dyskinetic mice, l-dopa injection induced dyskinesia to a similar or somewhat greater extent than optical stimulation. Combined l-dopa administration and stimulation resulted in an additive increase in dyskinesias, indicating that other mechanisms also contribute. Molecular studies indicate that changes in extracellular signal-regulated kinase phosphorylation in D1-expressing medium spiny neurons are involved. Optical stimulation did not ameliorate parkinsonism in l-dopa-naïve mice. However, it improved parkinsonism in l-dopa-primed mice to a similar extent as l-dopa administration. None of the stimulation paradigms enhanced dyskinesia or modified parkinsonism in l-dopa-naïve or l-dopa-primed control virus mice.
The data provide direct evidence that striatal D1-expressing medium spiny neuron stimulation is sufficient to induce dyskinesias and contributes to the regulation of motor control. © 2017 International Parkinson and Movement Disorder Society.
运动障碍是长期左旋多巴治疗引发的一种致残性运动并发症。使用D1受体药物和基因改造小鼠的研究表明,表达D1受体的中等棘状神经元在左旋多巴诱导的运动障碍中起主要作用。然而,这些神经元在运动障碍中的具体作用尚未完全明确。
我们采用光遗传学技术(该技术可在体内精确调节特定神经元)来研究纹状体中表达D1的中等棘状神经元活动是否调节帕金森病小鼠的异常不自主运动或运动障碍。用6-羟基多巴胺单侧损伤的D1-cre小鼠接受纹状体注射依赖于cre的通道视紫红质2病毒或对照病毒。在病毒稳定表达后,在未使用左旋多巴和已使用左旋多巴预处理的小鼠中测试光刺激对运动障碍的影响。
对表达D1的中等棘状神经元进行单脉冲和爆发式光刺激可在未使用左旋多巴的通道视紫红质2小鼠中诱发运动障碍。在稳定出现运动障碍的小鼠中,注射左旋多巴诱发运动障碍的程度与光刺激相似或略高。联合给予左旋多巴和刺激导致运动障碍呈累加性增加,表明还有其他机制起作用。分子研究表明,表达D1的中等棘状神经元中细胞外信号调节激酶磷酸化的变化与之有关。光刺激并未改善未使用左旋多巴小鼠的帕金森病症状。然而,它改善已使用左旋多巴预处理小鼠的帕金森病症状的程度与给予左旋多巴相似。在未使用左旋多巴或已使用左旋多巴预处理的对照病毒小鼠中,没有一种刺激模式会加重运动障碍或改变帕金森病症状。
数据提供了直接证据,表明纹状体中表达D1的中等棘状神经元刺激足以诱发运动障碍,并有助于运动控制的调节。©2017国际帕金森病和运动障碍协会。