Journal
MOLECULAR NEURODEGENERATION
Volume 8, Issue -, Pages -Publisher
BMC
DOI: 10.1186/1750-1326-8-14
Keywords
Parkinson's disease; 6-OHDA; Motor behavior; Emotion; Levodopa; Bupropion; Paroxetine
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Funding
- Fundacao Calouste de Gulbenkian
- Portuguese Foundation for Science and Technology [SFRH/BD/51061/2010, SFRH/BD/47311/2008, SFRH/BPD/33611/2009]
- Fundação para a Ciência e a Tecnologia [SFRH/BD/51061/2010, SFRH/BD/47311/2008, SFRH/BPD/33611/2009] Funding Source: FCT
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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.
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