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Updated: Mar 26, 2026

Generating Acute and Chronic Experimental Models of Motor Tic Expression in Rats
Published on: May 27, 2021
A Primary Role for Nucleus Accumbens and Related Limbic Network in Vocal Tics
Kevin W McCairn1, Yuji Nagai2, Yukiko Hori2
1Systems Neuroscience and Movement Disorders Laboratory, Korea Brain Research Institute, Daegu 701-300, South Korea; Laboratory for Symbolic Cognitive Development, RIKEN Brain Science Institute, Wako, Saitama 351-0198, Japan; Systems Neuroscience Section, Primate Research Institute, Kyoto University, Inuyama, Aichi 484-8506, Japan; Laboratory of Cognitive and Behavioral Neuroscience, Division of Biomedical Science, Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki 305-8577, Japan.
Abstract:
Inappropriate vocal expressions, e.g., vocal tics in Tourette syndrome, severely impact quality of life. Neural mechanisms underlying vocal tics remain unexplored because no established animal model representing the condition exists. We report that unilateral disinhibition of the nucleus accumbens (NAc) generates vocal tics in monkeys. Whole-brain PET imaging identified prominent, bilateral limbic cortico-subcortical activation. Local field potentials (LFPs) developed abnormal spikes in the NAc and the anterior cingulate cortex (ACC). Vocalization could occur without obvious LFP spikes, however, when phase-phase coupling of alpha oscillations were accentuated between the NAc, ACC, and the primary motor cortex. These findings contrasted with myoclonic motor tics induced by disinhibition of the dorsolateral putamen, where PET activity was confined to the ipsilateral sensorimotor system and LFP spikes always preceded motor tics. We propose that vocal tics emerge as a consequence of dysrhythmic alpha coupling between critical nodes in the limbic and motor networks. VIDEO ABSTRACT.
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