Ablation of the tail of the ventral tegmental area compensates symptoms in an experimental model of Parkinson's disease
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Other documents of the author: Faivre, Fanny; Sánchez-Catalán, María José; Dovero, Sandra; Bido, Simone; Joshi, Anil; Bezard, Erwan; Barrot, Michel
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Title
Ablation of the tail of the ventral tegmental area compensates symptoms in an experimental model of Parkinson's diseaseAuthor (s)
Date
2020Publisher
ElsevierISSN
0969-9961Bibliographic citation
FAIVRE, Fanny, et al. Ablation of the tail of the ventral tegmental area compensates symptoms in an experimental model of Parkinson's disease. Neurobiology of Disease, 2020, vol. 139, p. 104818.Type
info:eu-repo/semantics/articlePublisher version
https://www.sciencedirect.com/science/article/pii/S0969996120300930Version
info:eu-repo/semantics/publishedVersionSubject
Abstract
Parkinson's disease is a neurodegenerative disorder partly caused by the loss of the dopamine neurons of the nigrostriatal pathway. It is accompanied by motor as well as non-motor symptoms, including pain and depression. ... [+]
Parkinson's disease is a neurodegenerative disorder partly caused by the loss of the dopamine neurons of the nigrostriatal pathway. It is accompanied by motor as well as non-motor symptoms, including pain and depression. The tail of the ventral tegmental area (tVTA) or rostromedial tegmental nucleus (RMTg) is a GABAergic mesopontine structure that acts as a major inhibitory brake for the substantia nigra pars compacta (SNc) dopamine cells, thus controlling their neuronal activity and related motor functions. The present study tested the influence of suppressing this tVTA brake on motor and non-motor symptoms in a rat model of Parkinson's disease. Using behavioral approaches, we showed that male Sprague-Dawley rats with bilateral and partial 6-hydroxydopamine SNc lesion displayed motor impairments in the rotarod test, impairments that were no more present following a co-lesion of the tVTA. Using a larger set of behavioral tests, we then showed that such SNc lesion also led to non-motor symptoms, including lower body weight, lower mechanical nociceptive thresholds in the forceps test and lower thermal nociceptive thresholds in the incremented hot-plate test, and a decreased sucrose preference in a 2-bottle choice paradigm. The excitotoxic co-lesion of the tVTA led to compensation of body weight, mechanical nociceptive thresholds and anhedonia-like behavior. These findings illustrate the major influence that the tVTA exerts on the dopamine system, modulating the motor and non-motor symptoms related to a partial loss of dopamine cells. [-]
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Neurobiology of Disease, 2020, vol. 139.Investigation project
UPR3212, UMR5293, ANR-15-CE37-0005-02, Euridol ANR-17-EURE-0022, FDT20170437322, 24220Rights
info:eu-repo/semantics/openAccess
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