Gonda Multidisciplinary Brain Research Center, Bar-Ilan University, Ramat-Gan 52900, Israel.
Neurosci Biobehav Rev. 2013 Jul;37(6):1101-19. doi: 10.1016/j.neubiorev.2012.09.010. Epub 2012 Oct 23.
Pharmacological animal models of Tourette syndrome (TS) are an important tool for studying the neural mechanisms underlying this disorder. Dysfunction of the cortico-basal ganglia (CBG) system has been widely implicated in TS but the exact nature of this dysfunction is unknown. Pharmacological treatments of TS have prompted multiple hypotheses regarding the involvement of different neuromodulators in the disorder. Pharmacological manipulations in animal models were used to investigate the relationships between these neuromodulators and different symptoms of TS, including motor (tics) and non-motor (sensorimotor gating deficits) phenomena. Models initially focused on the direct effects of pharmacology on behavior, and only recently have begun providing neurophysiological data reflecting the neuronal mechanism linking the two. Animal models support the notion of CBG dysfunction as the neural mechanism underlying TS, and suggest that it may be derived from either direct deficits of local striatal GABAergic networks or a dysfunction of the neuromodulator systems controlling them. These findings can provide the much- needed conceptual construct for the TS etiology and point to new therapeutic targets.
抽动秽语综合征(TS)的药理学动物模型是研究该疾病神经机制的重要工具。皮质基底节(CBG)系统的功能障碍已被广泛认为与 TS 有关,但确切的功能障碍性质尚不清楚。TS 的药物治疗提出了多个关于不同神经调质参与该疾病的假设。动物模型中的药物操作用于研究这些神经调质与 TS 的不同症状(包括运动(抽搐)和非运动(感觉运动门控缺陷)现象)之间的关系。模型最初侧重于药理学对行为的直接影响,直到最近才开始提供反映连接两者的神经元机制的神经生理学数据。动物模型支持 CBG 功能障碍作为 TS 的神经机制的观点,并表明它可能源自局部纹状体 GABA 能网络的直接缺陷,或者是控制它们的神经调质系统的功能障碍。这些发现可以为 TS 的病因提供急需的概念结构,并指向新的治疗靶点。