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首页> 外文期刊>Cortex: A Journal Devoted to the Study of the Nervous System and Behavior >Towards a primate model of Gilles de la Tourette syndrome: Anatomo-behavioural correlation of disorders induced by striatal dysfunction
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Towards a primate model of Gilles de la Tourette syndrome: Anatomo-behavioural correlation of disorders induced by striatal dysfunction

机译：建立吉尔斯·德·图雷特综合症的灵长类动物模型：纹状体功能障碍所致疾病的解剖学与行为学相关性

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Introduction: Gilles de la Tourette syndrome (GTS) is characterized by abnormal movements (tics) often associated with behavioural disorders. Neuropathological data from GTS patients have suggested that aberrant activation of distinct striatal functional territories could produce a large spectrum of GTS symptoms. In a monkey model, injections of GABA-antagonist into the striatum enabled us to produce tic-like movements, hyperactivity and stereotyped behaviours. These effects had similarities with simple motor tics, hyperactivity and compulsive behaviours observed in GTS patients. In this study, we first aimed to identify the neuronal circuits involved in the different behavioural effects using anatomical antero/retrograde tracer in monkeys. We also compared the neuronal circuits thus obtained with the available neuro-anatomical data on GTS patients. Methods: Using injections of axonal tracer into different functional parts of the striatum of eight monkeys, we identified cortical, thalamic and basal ganglia regions related to the expression of tic-like movements, hyperactivity and stereotyped behaviours induced in response to microinjection of GABA-antagonist. Results: In this monkey model, different anatomical circuits involving distinct cortical and thalamic areas and sub-territories of the basal ganglia underpinned movement and behavioural disorders. Thus, tic-like movements were associated with neuronal labelling within the sensorimotor network, mostly in the medial and lateral premotor cortex and sensorimotor parts of the basal ganglia. Neuronal labelling in the prefrontal dorso-lateral cortex and associative territories of the basal ganglia was related to hyperactivity disorder and stereotyped behaviours were linked to the orbitofrontal cortex and limbic part of the basal ganglia. Conclusions: These results support the hypothesis that different behavioural effects could arise from distinct but inter-digitated neuronal circuits. As these behavioural disorders shared some similarities with simple motor tics, hyperactivity and compulsive behaviours observed in GTS patients, this model could be a good tool for future studies involving the modulation of neuronal circuits, such as deep brain stimulation.
机译：简介：吉尔斯·图拉·图雷特综合症（GTS）的特征是经常与行为障碍相关的异常动作（抽动）。来自GTS患者的神经病理学数据表明，不同纹状体功能区域的异常激活可能产生大量GTS症状。在猴子模型中，向纹状体注射GABA拮抗剂使我们能够产生抽动样运动，活动亢进和刻板行为。这些作用与在GTS患者中观察到的简单运动，多动和强迫行为相似。在这项研究中，我们首先旨在使用猴子的解剖前/逆行示踪剂识别参与不同行为影响的神经元回路。我们还将获得的神经元回路与GTS患者的可用神经解剖数据进行了比较。方法：通过向八只猴子的纹状体不同功能部位注射轴突示踪剂，我们鉴定了皮质，丘脑和基底神经节区域，这些区域与微注射GABA拮抗剂诱导的抽动样运动，过度活跃和刻板行为的表达有关。结果：在这个猴子模型中，涉及不同的皮层和丘脑区域以及基底神经节的子区域的不同解剖回路支撑了运动和行为障碍。因此，抽动样运动与感觉运动网络内的神经元标记有关，主要是在运动前皮层的内侧和外侧以及基底神经节的感觉运动部分。基底节的前额外侧皮层和相关区域的神经元标记与多动障碍有关，刻板行为与基底节的眶额皮质和边缘部分有关。结论：这些结果支持以下假设：不同但相互交叉的神经元回路可能产生不同的行为影响。由于这些行为障碍与在GTS患者中观察到的简单运动，活动亢进和强迫行为具有某些相似之处，因此该模型可能是将来涉及神经回路调节（例如深部脑刺激）的研究的良好工具。

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