In vivo evidence for GABAA receptor changes in the sensorimotor system in primary dystonia
Identifieur interne : 001622 ( Main/Exploration ); précédent : 001621; suivant : 001623In vivo evidence for GABAA receptor changes in the sensorimotor system in primary dystonia
Auteurs : Valentina Garibotto [Italie] ; Luigi M. Romito [Italie] ; Antonio E. Elia [Italie] ; Paola Soliveri [Italie] ; Andrea Panzacchi [Italie] ; Assunta Carpinelli [Italie] ; Michele Tinazzi [Italie] ; Alberto Albanese [Italie] ; Daniela Perani [Italie]Source :
- Movement Disorders [ 0885-3185 ] ; 2011-04.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Adult, Analysis of Variance, Brain Mapping, Cerebral Cortex (metabolism), Cerebral Cortex (radionuclide imaging), Dystonia, Dystonic Disorders (diagnosis), Dystonic Disorders (genetics), Dystonic Disorders (pathology), Dystonic Disorders (radionuclide imaging), Emission tomography, Female, Flumazenil (pharmacokinetics), GABA, GABA Modulators (pharmacokinetics), GABAA receptors, Gabaergic receptor A, Humans, Male, Middle Aged, Molecular Chaperones (genetics), Nervous system diseases, PET, Positron emission tomography, Receptors, GABA-A (metabolism), Sensorimotor cortex, Sequence Deletion (genetics), Trinucleotide Repeats (genetics), dystonia, sensorimotor cortex.
- MESH :
- chemical , genetics : Molecular Chaperones.
- chemical , metabolism : Receptors, GABA-A.
- chemical , pharmacokinetics : Flumazenil, GABA Modulators.
- diagnosis : Dystonic Disorders.
- genetics : Dystonic Disorders, Sequence Deletion, Trinucleotide Repeats.
- metabolism : Cerebral Cortex.
- pathology : Dystonic Disorders.
- radionuclide imaging : Cerebral Cortex, Dystonic Disorders.
- Adult, Analysis of Variance, Brain Mapping, Female, Humans, Male, Middle Aged.
Abstract
Background:: Preclinical and clinical evidence suggests that impaired gamma‐aminobutyric (GABA) control, leading to disinhibition within the sensorimotor system, might play a role in dystonia. Aim of this study is the in vivo assessment of the GABAergic system in dystonia using positron emission tomography (PET) and 11C‐flumazenil, a selective GABAA receptor ligand. Methods:: Fourteen subjects with primary dystonia (9 carriers of the DYT1 mutation and 5 sporadic cases) were compared to 11 controls, using a simplified reference tissue model to measure binding potential. Results:: Voxel‐based analyses showed a reduction in GABAA receptor expression/affinity both in DYT1 carriers and sporadic patients in primary motor and premotor cortex, primary and secondary somatosensory cortex, and in the motor component of the cingulate gyrus. Conclusions:: Dysfunction of GABAA receptors in sensorimotor systems in primary (genetic and sporadic) dystonia supports the view that lack of GABAergic control may be associated with the generation of dystonic movements. © 2011 Movement Disorder Society
Url:
DOI: 10.1002/mds.23553
Affiliations:
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Le document en format XML
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<term>Cerebral Cortex (radionuclide imaging)</term>
<term>Dystonia</term>
<term>Dystonic Disorders (diagnosis)</term>
<term>Dystonic Disorders (genetics)</term>
<term>Dystonic Disorders (pathology)</term>
<term>Dystonic Disorders (radionuclide imaging)</term>
<term>Emission tomography</term>
<term>Female</term>
<term>Flumazenil (pharmacokinetics)</term>
<term>GABA</term>
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<term>GABAA receptors</term>
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<term>Humans</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Molecular Chaperones (genetics)</term>
<term>Nervous system diseases</term>
<term>PET</term>
<term>Positron emission tomography</term>
<term>Receptors, GABA-A (metabolism)</term>
<term>Sensorimotor cortex</term>
<term>Sequence Deletion (genetics)</term>
<term>Trinucleotide Repeats (genetics)</term>
<term>dystonia</term>
<term>sensorimotor cortex</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Dystonic Disorders</term>
<term>Sequence Deletion</term>
<term>Trinucleotide Repeats</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cerebral Cortex</term>
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<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Dystonic Disorders</term>
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<term>Humans</term>
<term>Male</term>
<term>Middle Aged</term>
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<term>Dystonie</term>
<term>GABA</term>
<term>Pathologie du système nerveux</term>
<term>Récepteur gabaergique A</term>
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<front><div type="abstract" xml:lang="en">Background:: Preclinical and clinical evidence suggests that impaired gamma‐aminobutyric (GABA) control, leading to disinhibition within the sensorimotor system, might play a role in dystonia. Aim of this study is the in vivo assessment of the GABAergic system in dystonia using positron emission tomography (PET) and 11C‐flumazenil, a selective GABAA receptor ligand. Methods:: Fourteen subjects with primary dystonia (9 carriers of the DYT1 mutation and 5 sporadic cases) were compared to 11 controls, using a simplified reference tissue model to measure binding potential. Results:: Voxel‐based analyses showed a reduction in GABAA receptor expression/affinity both in DYT1 carriers and sporadic patients in primary motor and premotor cortex, primary and secondary somatosensory cortex, and in the motor component of the cingulate gyrus. Conclusions:: Dysfunction of GABAA receptors in sensorimotor systems in primary (genetic and sporadic) dystonia supports the view that lack of GABAergic control may be associated with the generation of dystonic movements. © 2011 Movement Disorder Society</div>
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