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5-羟色胺转运体抑制可减轻左旋多巴诱导的异动症,而不影响半帕金森病大鼠的左旋多巴疗效。

Serotonin transporter inhibition attenuates l-DOPA-induced dyskinesia without compromising l-DOPA efficacy in hemi-parkinsonian rats.

机构信息

Behavioral Neuroscience Program, Department of Psychology, Binghamton University, 4400 Vestal Parkway East, Binghamton, NY 13902-6000, USA.

出版信息

Eur J Neurosci. 2012 Sep;36(6):2839-48. doi: 10.1111/j.1460-9568.2012.08202.x. Epub 2012 Jul 5.

Abstract

Long-term dopamine replacement therapy with l-DOPA in Parkinson's disease often leads to the development of abnormal involuntary movements known as l-DOPA-induced dyskinesia. Growing evidence suggests that, following dopamine cell loss, serotonin neurons acting as surrogates for dopaminergic processes take up l-DOPA, convert it to dopamine and release it in an unregulated fashion that precipitates dyskinesia. Although most studies have focused on serotonin 5-HT(1) receptor stimulation as an antidyskinetic strategy, targeting the serotonin transporter modulation of dopamine activity has been overlooked. Therefore, in the current study, selective serotonin reuptake inhibitors were tested for their ability to reduce l-DOPA- and apomorphine-induced dyskinesia. In Experiments 1 and 2, hemi-parkinsonian rats were primed with l-DOPA until stable dyskinesia developed. Rats in Experiment 1 were administered the selective serotonin reuptake inhibitors paroxetine, citalopram or fluoxetine, followed by l-DOPA. Abnormal involuntary movements and forepaw adjusting steps were recorded to determine the effects of these compounds on dyskinesia and motor performance, respectively. Brains were collected on the final test day, after which striatal and raphe monoamines were examined via high-performance liquid chromatography. In Experiment 2, dyskinesias were measured after selective serotonin reuptake inhibitors and apomorphine. Serotonin reuptake inhibitors dose-dependently attenuated l-DOPA- but not apomorphine-induced dyskinesia, and preserved l-DOPA efficacy. Neurochemically, serotonin transporter inhibition enhanced striatal and raphe serotonin levels and reduced its turnover, indicating a potential mechanism of action. The present results support targeting serotonin transporters to improve Parkinson's disease treatment and provide further evidence for the role of the serotonin system in l-DOPA's effects.

摘要

长期应用左旋多巴(L-DOPA)治疗帕金森病常常导致异常不自主运动的发生,这种运动障碍称为左旋多巴诱导的运动障碍(LID)。越来越多的证据表明,在多巴胺能神经元丧失后,作为多巴胺能过程替代物的 5-羟色胺(5-HT)能神经元摄取 L-DOPA,将其转化为多巴胺并以不受调节的方式释放,从而引发运动障碍。虽然大多数研究都集中在 5-HT1 受体刺激作为抗运动障碍的策略上,但对 5-HT 转运体调节多巴胺活性的靶向作用却被忽视了。因此,在本研究中,我们测试了选择性 5-HT 再摄取抑制剂减少 L-DOPA 和阿朴吗啡诱导的运动障碍的能力。在实验 1 和 2 中,半帕金森大鼠接受 L-DOPA 预处理,直到稳定出现运动障碍。实验 1 中的大鼠给予选择性 5-HT 再摄取抑制剂帕罗西汀、西酞普兰或氟西汀,然后给予 L-DOPA。记录异常不自主运动和前爪调整步数,以确定这些化合物对运动障碍和运动表现的影响。在最后一次测试日收集大脑,然后通过高效液相色谱法检测纹状体和中缝核单胺类物质。在实验 2 中,在给予选择性 5-HT 再摄取抑制剂和阿朴吗啡后测量运动障碍。选择性 5-HT 再摄取抑制剂呈剂量依赖性地减轻 L-DOPA 但不减轻阿朴吗啡诱导的运动障碍,并保留 L-DOPA 的疗效。神经化学研究表明,5-HT 转运体抑制增强了纹状体和中缝核的 5-HT 水平,并降低了其周转率,表明其潜在的作用机制。本研究结果支持靶向 5-HT 转运体以改善帕金森病的治疗,并为 5-HT 系统在 L-DOPA 作用中的作用提供了进一步的证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63e4/3445783/3492de76f54d/nihms383705f1a.jpg

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