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5-HT(1A) receptor activation improves anti-cataleptic effects of levodopa in 6-hydroxydopamine-lesioned rats.5-HT(1A) 受体激动剂可增强左旋多巴对 6-羟多巴胺损毁大鼠的抗僵直作用。
Daru. 2011;19(5):338-43.
2
Buspirone improves haloperidol-induced Parkinson disease in mice through 5-HT(1A) recaptors.丁螺环酮通过 5-HT(1A) 再摄取受体改善小鼠的氟哌啶醇诱导的帕金森病。
Daru. 2010;18(1):41-5.
3
Buspirone improves the anti-cataleptic effect of levodopa in 6-hydroxydopamine-lesioned rats.丁螺环酮增强左旋多巴对 6-羟多巴胺损毁大鼠的抗僵住作用。
Pharmacol Rep. 2011;63(4):908-14. doi: 10.1016/s1734-1140(11)70606-5.
4
Buspirone improves 6-hydroxydopamine-induced catalepsy through stimulation of nigral 5-HT(1A) receptors in rats.丁螺环酮通过刺激大鼠黑质 5-HT(1A)受体改善 6-羟多巴胺诱导的僵住症。
Pharmacol Rep. 2010 Mar-Apr;62(2):258-64. doi: 10.1016/s1734-1140(10)70264-4.
5
Role of serotonin neurons in the induction of levodopa- and graft-induced dyskinesias in Parkinson's disease.5-羟色胺能神经元在左旋多巴诱导和移植诱导的帕金森病运动障碍中的作用。
Mov Disord. 2010;25 Suppl 1:S174-9. doi: 10.1002/mds.22792.
6
Levodopa in the early treatment of Parkinson's disease.左旋多巴在帕金森病早期治疗中的应用
Parkinsonism Relat Disord. 2009 Jan;15 Suppl 1:S17-20. doi: 10.1016/S1353-8020(09)70006-9.
7
Combined 5-HT1A and 5-HT1B receptor agonists for the treatment of L-DOPA-induced dyskinesia.联合5-HT1A和5-HT1B受体激动剂治疗左旋多巴诱导的运动障碍。
Brain. 2008 Dec;131(Pt 12):3380-94. doi: 10.1093/brain/awn235. Epub 2008 Oct 24.
8
Involvement of the serotonin system in L-dopa-induced dyskinesias.血清素系统与左旋多巴诱发的运动障碍的关系。
Parkinsonism Relat Disord. 2008;14 Suppl 2:S154-8. doi: 10.1016/j.parkreldis.2008.04.021. Epub 2008 Jun 24.
9
Animal models of Parkinson's disease and L-dopa induced dyskinesia: how close are we to the clinic?帕金森病和左旋多巴诱发的运动障碍的动物模型：我们离临床应用还有多远？
Psychopharmacology (Berl). 2008 Aug;199(3):303-12. doi: 10.1007/s00213-007-0931-8. Epub 2007 Sep 25.
10
Serotonin neuron transplants exacerbate L-DOPA-induced dyskinesias in a rat model of Parkinson's disease.在帕金森病大鼠模型中，5-羟色胺能神经元移植会加重左旋多巴诱导的运动障碍。
J Neurosci. 2007 Jul 25;27(30):8011-22. doi: 10.1523/JNEUROSCI.2079-07.2007.

通过5HT1A受体抑制血清素能系统是治疗左旋多巴诱导的运动问题的一个有前景的靶点。

Dampening of Serotonergic System through 5HT1A Receptors is a Promising Target for Treatment of Levodopa Induced Motor Problems.

作者信息

Mahmoudi Javad, Farhoudi Mehdi, Reyhani-Rad Siamak, Sadigh-Eteghad Saeed

机构信息

Neurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, Iran.

出版信息

Adv Pharm Bull. 2013;3(2):439-41. doi: 10.5681/apb.2013.071. Epub 2013 Aug 20.

DOI:10.5681/apb.2013.071
PMID:24312874
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3848224/
Abstract

During long-term treatment with Levodopa, majority of patients with Parkinson's disease experience some abnormal motor problems including of Levodopa induced dyskinesia (LID) and wearing off. Incredible evidences suggest that serotonergic neurons compensate some functions of lost dopaminergic neurons in Parkinson's disease especially in advanced disease stages. Therefore, it has been postulated that serotonergic neurons are the major source for development of these unwanted effects. 5HT1A receptors are located on the serotonergic neurons and are involved in regulation of normal motor functions. With respect to the role of serotonergic projection in Parkinson's disease and importance of 5HT1A receptors in motor activity it seems that inactivation of these neurons by stimulation of 5HT1A receptors could provide benefits in treatment of Levodopa induced motor impairments.

摘要

在长期使用左旋多巴治疗期间，大多数帕金森病患者会出现一些异常运动问题，包括左旋多巴诱发的异动症（LID）和疗效减退。大量证据表明，5-羟色胺能神经元可代偿帕金森病中丧失的多巴胺能神经元的某些功能，尤其是在疾病晚期。因此，有人推测5-羟色胺能神经元是这些不良反应发生的主要来源。5-HT1A受体位于5-羟色胺能神经元上，参与正常运动功能的调节。鉴于5-羟色胺能投射在帕金森病中的作用以及5-HT1A受体在运动活动中的重要性，通过刺激5-HT1A受体使这些神经元失活似乎可能对治疗左旋多巴诱发的运动障碍有益。