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Related Experiment Video

Updated: Jun 15, 2026

Generating Acute and Chronic Experimental Models of Motor Tic Expression in Rats

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Extrastriatal dopaminergic dysfunction in tourette syndrome.

Thomas D L Steeves¹, Ji Hyun Ko, David M Kideckel

¹Division of Neurology, Toronto Western Hospital, University Health Network, University of Toronto, Ontario, Canada.

Annals of Neurology

|March 13, 2010

Summary

Tourette syndrome patients exhibit altered dopamine D2/D3 receptor binding and release in brain regions outside the striatum. These dopaminergic abnormalities may explain thalamocortical circuit hyperexcitability in Tourette syndrome.

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Area of Science:

Neuroscience
Psychiatry
Radiology

Background:

Tourette syndrome (TS) involves tics and non-motor symptoms like ADHD and OCD.
Dopaminergic system dysfunction is implicated in TS pathogenesis.
Evidence suggests brain regions beyond the striatum are involved in tic generation.

Purpose of the Study:

To investigate extrastriatal dopamine D2/D3 receptor binding and release in adult Tourette syndrome patients.
To compare dopamine dynamics in treatment-naive TS patients with healthy controls using PET imaging and amphetamine challenge.

Main Methods:

Utilized [11C]FLB 457 positron emission tomography (PET) for imaging.
Administered an amphetamine challenge to assess dopamine release.
Compared PET data from adult, treatment-naive TS patients and age/sex-matched controls.

Main Results:

TS patients showed reduced [11C]FLB 457 binding in extrastriatal regions (e.g., cingulate, temporal cortex, insula, thalamus).
Amphetamine challenge revealed more widespread and anterior dopamine release in TS patients compared to controls.
Thalamic dopamine release was absent in TS patients, unlike in controls.

Conclusions:

Dopaminergic abnormalities in TS are localized to implicated brain regions.
Findings suggest a mechanism for thalamocortical circuit hyperexcitability in Tourette syndrome.
Extrastriatal dopaminergic system alterations are key in Tourette syndrome pathophysiology.