Tourette syndrome (TS) and attention deficit hyperactivity disorder (ADHD) are two neurodevelopmental hyper-behavioral disorders that are highly comorbid. The source of this comorbidity and the neuronal mechanisms underlying these disorders are still unclear. We examined the neuronal activity of freely behaving rats before and after striatal disinhibition, to reveal the similar and distinct neuronal components underlying the mechanisms of TS-like and ADHD-like symptom expression. Focal disinhibition induced motor tics, locomotor hyperactivity or a comorbid effect depending on the location of the injection within the different functional domains of the striatum. While injections within the motor domain induced motor tics, injections into the limbic domain induced mainly locomotor hyperactivity. Disinhibition, regardless of its striatal location, led to qualitatively similar macro-scale and micro-scale neuronal changes. These changes were localized to the domain of the manipulation and remained partly segregated, indicating that hyperactivity is induced as a result of changes in the limbic domain without directly activating the motor domain. Despite the general similarity of induced neuronal changes, these changes were associated with different behavioral effects and were more stereotypic and pronounced following motor-domain disinhibition in comparison to limbic-domain disinhibition. Our recordings revealed a disparity in the neuronal input-output transformation of the two models of the disorders. The results suggest that tic expression and hyperactivity states share similar local neuronal activity changes which manifest in different neuronal and behavioral outcomes. These results expose an intriguing link between tics and their comorbid symptoms and hint at striatal disinhibition, resulting from GABAergic alterations, as a potential common mechanism underlying distinct symptoms expressed by hyper-behavioral patients.

中文翻译：

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抽动和多动症的常见神经元机制。

抽动秽语综合征（TS）和注意力缺陷多动障碍（ADHD）是两种高度共病的神经发育过度行为障碍。这种合并症的来源和这些疾病的神经机制尚不清楚。我们检查了纹状体去抑制前后自由行为的大鼠的神经元活动，以揭示潜在的类似TS和ADHD症状表达机制的相似和不同的神经元成分。根据注射在纹状体不同功能域内的位置，局灶性抑制引起运动性抽动，运动过度活跃或合并症。在运动域内注射引起运动性抽动，而向边缘域的注射主要引起运动亢进。禁忌症，无论其纹状体位置如何，导致定性相似的宏观和微观神经元变化。这些变化位于操作区域，并保持部分隔离，这表明由于边缘区域的变化而导致过度活跃，而没有直接激活运动区域。尽管诱导的神经元变化具有普遍相似性，但与边缘域抑制相比，这些变化与不同的行为效应相关，并且在运动域抑制作用下更加刻板且明显。我们的录音揭示了两种疾病模型在神经元输入输出转换方面的差异。结果表明抽动表达和多动状态共享相似的局部神经元活动变化，这表现在不同的神经元和行为结果中。