Tourette syndrome research highlights from 2016

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Abstract

This article presents highlights chosen from research that appeared during 2016 on Tourette syndrome and other tic disorders. Selected articles felt to represent meaningful advances in the field are briefly summarized.

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Most cited references 85

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Neurobiology of rodent self-grooming and its value for translational neuroscience.

Allan V. Kalueff, Adam Stewart, Cai Song … (2016)

Self-grooming is a complex innate behaviour with an evolutionarily conserved sequencing pattern and is one of the most frequently performed behavioural activities in rodents. In this Review, we discuss the neurobiology of rodent self-grooming, and we highlight studies of rodent models of neuropsychiatric disorders--including models of autism spectrum disorder and obsessive compulsive disorder--that have assessed self-grooming phenotypes. We suggest that rodent self-grooming may be a useful measure of repetitive behaviour in such models, and therefore of value to translational psychiatry. Assessment of rodent self-grooming may also be useful for understanding the neural circuits that are involved in complex sequential patterns of action.

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Altered parvalbumin-positive neuron distribution in basal ganglia of individuals with Tourette syndrome.

Clifford B. Saper, Wei-Zheng, Jana Schwartz … (2005)

Tourette syndrome (TS) is a childhood neuropsychiatric disorder characterized by motor and vocal tics. Imaging studies found alterations in caudate (Cd) and putamen volumes. To investigate possible alterations in cell populations, postmortem basal ganglia tissue from individuals with TS and normal controls was analyzed by using unbiased stereological techniques. A markedly higher total neuron number was found in the globus pallidus pars interna (GPi) of TS. In contrast, a lower neuron number and density was observed in the globus pallidus pars externa and in the Cd. An increased number and proportion of the GPi neurons were positive for the calcium-binding protein parvalbumin in tissue from TS subjects, whereas lower densities of parvalbumin-positive interneurons were observed in both the Cd and putamen of TS subjects. This change is consistent with a developmental defect in tangential migration of some GABAergic neurons. The imbalance in striatal and GPi inhibitory neuron distribution suggests that the functional dynamics of cortico-striato-thalamic circuitry are fundamentally altered in severe, persistent TS.

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Decreased number of parvalbumin and cholinergic interneurons in the striatum of individuals with Tourette syndrome.

Clifford B. Saper, Heidi Grantz, Jana Schwartz … (2010)

Corticobasal ganglia neuronal ensembles bring automatic motor skills into voluntary control and integrate them into ongoing motor behavior. A 5% decrease in caudate (Cd) nucleus volume is the most consistent structural finding in the brain of patients with Tourette syndrome (TS), but the cellular abnormalities that underlie this decrease in volume are unclear. In this study the density of different types of interneurons and medium spiny neurons (MSNs) in the striatum was assessed in the postmortem brains of 5 TS subjects as compared with normal controls (NC) by unbiased stereological analyses. TS patients demonstrated a 50%-60% decrease of both parvalbumin (PV)+ and choline acetyltransferase (ChAT)+ cholinergic interneurons in the Cd and the putamen (Pt). Cholinergic interneurons were decreased in TS patients in the associative and sensorimotor regions but not in the limbic regions of the striatum, such that the normal gradient in density of cholinergic cells (highest in associative regions, intermediate in sensorimotor and lowest in limbic regions) was abolished. No significant difference was present in the densities of medium-sized calretinin (CR)+ interneurons, MSNs, and total neurons. The selective deficit of PV+ and cholinergic striatal interneurons in TS subjects may result in an impaired cortico/thalamic control of striatal neuron firing in TS.

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Author and article information

Contributors

Kevin J. Black: Role: InvestigationRole: Writing – Original Draft PreparationRole: Writing – Review & Editing

ORCID: https://orcid.org/0000-0002-6921-9567

Journal

Journal ID (nlm-ta): F1000Res

Journal ID (iso-abbrev): F1000Res

Journal ID (pmc): F1000Research

Title: F1000Research

Publisher: F1000Research (London, UK )

ISSN (Electronic): 2046-1402

Publication date (Electronic): 11 August 2017

Publication date Collection: 2017

Volume: 6

Electronic Location Identifier: 1430

Affiliations

[1 ]Departments of Psychiatry, Neurology, Radiology, and Neuroscience, Washington University School of Medicine, St. Louis, MO, 63110, USA

[1 ]Department of Neurology, Charité, University Medicine Berlin, Berlin, Germany

[1 ]University of Calgary, Calgary, AB, Canada

Department of Psychiatry, Washington University in St Louis, USA

[1 ]Child Psychiatry, Psychiatry, Psychology and Pediatrics, Yale Child Study Center, Yale School of Medicine, New Haven, CT, USA

Department of Psychiatry, Washington University in St Louis, USA

[1 ]Division of Pediatric Neurology, Department of Pediatrics, Children's Mercy Hospital, Kansas City, MO, USA

Department of Psychiatry, Washington University in St Louis, USA

Author notes

[a ] kevin@ 123456wustl.edu

Competing interests: KJB participated in clinical trials supported by Psyadon Pharmaceuticals and Neurocrine Biosciences, Inc.

Competing interests: No competing interests were disclosed.

Competing interests: I am a co-author of each of the articles that I have suggested that Dr. Black cite in his review.

Competing interests: No competing interests were disclosed.

Author information

Kevin J. Black https://orcid.org/0000-0002-6921-9567

Article

DOI: 10.12688/f1000research.12330.1

PMC ID: 5621096

SO-VID: f7b6142e-8642-4195-bab9-a899e7f05277

License:

This is an open access article distributed under the terms of the Creative Commons Attribution Licence, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date accepted : 10 August 2017

Funding

Funded by: National Institutes of Health

Award ID: R21NS091635

Award ID: R01MH104030

Funded by: Tourette Association of America

This work was supported in part by the U.S. National Institutes of Health (NIH) (grants R21 NS091635 and R01 MH104030), and by a research grant from the Tourette Association of America (PI: Cheryl A. Richards, Ph.D.).

The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

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Tourette syndrome research highlights from 2016

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Most cited references 85

Neurobiology of rodent self-grooming and its value for translational neuroscience.

Altered parvalbumin-positive neuron distribution in basal ganglia of individuals with Tourette syndrome.

Decreased number of parvalbumin and cholinergic interneurons in the striatum of individuals with Tourette syndrome.

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