http://www.cnr.it/ontology/cnr/individuo/prodotto/ID10525
In vivo evidence for GABA(A) receptor changes in the sensorimotor system in primary dystonia. (Articolo in rivista)
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- In vivo evidence for GABA(A) receptor changes in the sensorimotor system in primary dystonia. (Articolo in rivista) (literal)
- Anno
- 2011-01-01T00:00:00+01:00 (literal)
- Alternative label
Garibotto V. 1,2,3, Romito L.M. 4,5, Elia A.E. 4,5, Soliveri P. 4, Panzacchi A. 2,3, Carpinelli A. 6, Tinazzi M. 7,8, Albanese A. 4,5, Perani D. 1,2,3 (2011)
In vivo evidence for GABA(A) receptor changes in the sensorimotor system in primary dystonia.
in Movement disorders
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Garibotto V. 1,2,3, Romito L.M. 4,5, Elia A.E. 4,5, Soliveri P. 4, Panzacchi A. 2,3, Carpinelli A. 6, Tinazzi M. 7,8, Albanese A. 4,5, Perani D. 1,2,3 (literal)
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- Pubblicato on-line: 2 Marzo 2011
Corresponding author: D. Perani (daniela.perani@hsr.it)
IF 2010: 4.480 (literal)
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- ISI Web of Science (WOS) (literal)
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- 1. Division of Neuroscience, Vita-Salute San Raffaele University, Milano.
2. Division of Neuroscience, San Raffaele Scientific Institute, Milano.
3. Nuclear Medicine Unit, San Raffaele Scientific Institute, Milano.
4. Department of Neurology I, IRCCS Istituto Neurologico \"Carlo Besta\", Milano.
5. Neurology Institute, Università Cattolica del Sacro Cuore, Milano.
6. IBFM-CNR, Milano.
7. Department of Neurological and Visual Sciences, University of Verona, Verona.
8. Department of Neurology, Borgo Trento Hospital, Verona. (literal)
- Titolo
- In vivo evidence for GABA(A) receptor changes in the sensorimotor system in primary dystonia. (literal)
- 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. (literal)
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