Please use this identifier to cite or link to this item: http://hdl.handle.net/1822/25090

TitleBehavioral characterization of the 6-hydroxidopamine model of Parkinson's disease and pharmacological rescuing of non-motor deficits
Author(s)Carvalho, Miguel
Campos, Filipa L.
Coimbra, Bárbara Guimarães Salazar
Pêgo, José M.
Lima, Rui
Rodrigues, Ana João
Sousa, Nuno
Salgado, A. J.
KeywordsParkinson’s disease
6-OHDA
Motor behavior
Emotion
Levodopa
Bupropion
Paroxetine
Issue date22-Apr-2013
PublisherBioMed Central
JournalMolecular Neurodegeneration
Abstract(s)BACKGROUND: Parkinson's disease (PD) is a chronic neurodegenerative condition that is characterized by motor symptoms as a result of dopaminergic degeneration, particularly in the mesostriatal pathway. However, in recent years, a greater number of clinical studies have focused on the emergence of non-motor symptoms in PD patients, as a consequence of damage on the mesolimbic and mesocortical dopaminergic networks, and on their significant impact on the quality of life of PD patients. Herein, we performed a thorough behavioral analysis including motor, emotional and cognitive dimensions, of the unilateral medial forebrain bundle (MFB) 6-hydroxidopamine (6-OHDA)-lesioned model of PD, and further addressed the impact of pharmacological interventions with levodopa and antidepressants on mood dimensions. RESULTS: Based on apomorphine-induced turning behaviour and degree of dopaminergic degeneration, animals submitted to MFB lesions were subdivided in complete and incomplete lesion groups. Importantly, this division also translated into a different severity of motor and exploratory impairments and depressive-like symptoms; in contrast, no deficits in anxiety-like and cognitive behaviors were found in MFB-lesioned animals. Subsequently, we found that the exploratory and the anhedonic behavioural alterations of MFB-lesioned rats can be partially improved with the administration of both levodopa or the antidepressant bupropion, but not paroxetine. CONCLUSIONS: Our results suggest that this model is a relevant tool to study the pathophysiology of motor and non-motor symptoms of PD. In addition, the present data shows that pharmacological interventions modulating dopaminergic transmission are also relevant to revert the non-motor behavioral deficits found in the disease.
TypeArticle
URIhttp://hdl.handle.net/1822/25090
DOI10.1186/1750-1326-8-14
ISSN1750-1326
Publisher versionhttp://www.biomedcentral.com/
Peer-Reviewedyes
AccessOpen access
Appears in Collections:ICVS - Artigos em Revistas Internacionais com Referee

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