Decreased number of parvalbumin and cholinergic interneurons in the striatum of individuals with Tourette syndrome
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 ab...
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Published in | Journal of comparative neurology (1911) Vol. 518; no. 3; pp. 277 - 291 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01.02.2010
Wiley Subscription Services, Inc |
Subjects | |
Online Access | Get full text |
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Summary: | 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. J. Comp. Neurol. 518:277–291, 2010. © 2009 Wiley‐Liss, Inc. |
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Bibliography: | National Institutes of Health - No. R01NS054994; No. K05MH076273 ArticleID:CNE22206 istex:1A1C484EAD5C30C9FC28C0658D492D31DA6FA1B8 ark:/67375/WNG-GX5VPT2W-G Tourette Syndrome Association ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 ObjectType-Article-2 ObjectType-Feature-1 |
ISSN: | 0021-9967 1096-9861 1096-9861 |
DOI: | 10.1002/cne.22206 |