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Decreased platelet vesicular monoamine transporter binding capacity in tourette syndrome

Published online by Cambridge University Press:  16 April 2020

D.H. Ben-Dor
Affiliation:
Adolescent Unit, Geha Mental Health Center, Rabin Medical Center, Beilinson Campus, Petach Tikva, Israel
S. Zimerman
Affiliation:
Schneider Children's Medical Center of Israel, Petach Tikva, Israel
Y. Sever
Affiliation:
Adolescent Unit, Geha Mental Health Center, Rabin Medical Center, Beilinson Campus, Petach Tikva, Israel
N. Roz
Affiliation:
Department of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
A. Apter
Affiliation:
Schneider Children's Medical Center of Israel, Petach Tikva, Israel
M. Rehavi
Affiliation:
Department of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
A. Weizman
Affiliation:
Adolescent Unit, Geha Mental Health Center, Rabin Medical Center, Beilinson Campus, Petach Tikva, Israel

Abstract

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Background and aims:

The vesicular monoamine transporter (VMAT2) plays a major role in the synaptic accumulation and release of monoamines.

Methods:

We assessed high affinity [3H]dihydrotetrabenazine binding to platelet VMAT2, in a group of untreated male Tourette's syndrome (TS) patients (age: 8-17.5 years, n=9) and in a comparison group of age-and sex-matched healthy controls (age: 9-16 years, n=16).

Results:

Significantly decreased platelet VMAT2 density (Bmax) (-23%, P=0.016) was observed in the TS patients. The affinity (Kd) of the ligand to platelet VMAT2 was similar in both groups.

Conclusions:

If the lower platelet VMAT2 density also occured in the brain, it may serve as an adaptive mechanism geared to decrease dopamine storage in the presynaptic neurons and thereby to diminish the dopaminergic overactivity and ameliorate the movement disorder.

Type
Poster Session 2: Organic Mental Disorders and Memory and Cognitive Dysfunctions
Copyright
Copyright © European Psychiatric Association 2007
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