Name: Willyan Franco Hilario
Type: MSc dissertation
Publication date: 05/08/2015
Advisor:

Namesort descending Role
Rita Gomes Wanderley Pires Advisor *

Examining board:

Namesort descending Role
Cristina Martins e Silva Co advisor *
Ester Miyuki Nakamura Palacios External Examiner *
Lívia Carla de Melo Rodrigues External Examiner *
Rita Gomes Wanderley Pires Advisor *

Summary: Parkinson's disease (PD) is the second most common neurodegenerative disease in the world, characterized by dopaminergic neurodegeneration of substantia nigra pars compacta (SNpc). Although PD has been defined primarily like a motor disorder, currently a wide range of evidences has shown cognitive impairment in PD patients. Frequently, the cognitive impairment has been described in early stages of PD, even before the motor abnormalities and increases with the disease progression. The pharmacotherapy of PD has been based on replacement of the striatal dopamine (DA) levels with the dopaminergic precursor L-DOPA and/or dopaminergic agonists in order to mitigate the motor abnormalities. However, this pharmacotherapy neither prevents the disease progression nor reduces the cognitive impairments in these patients. The enriched environment (EE) is a paradigm that has been effective in preventing of several neurodegenerative processes, mainly in experimental models. The EE consists on the manipulation of the housing conditions, exposes the animals to diverse cognitive, motor and somatosensory stimuli. Several studies have demonstrated that EE induces morphological, biochemical and molecular changes, reflected in cognitive enhancing, neuroprotection and attenuation of stress, anxiety and depression effects. In this study, we investigated whether EE could prevent the motor, cognitive, biochemical and molecular abnormalities in a murine model of PD, induced by the drug 1-metil -4-fenil-1,2,3,6-tetrahydropyridine (MPTP). The EE prevented completely the muscle strength deficit and the hyperlocomotion induced by MPTP. Our biochemical data show that EE did not prevent the dopaminergic striatal depletion MPTP-induced, however, it was able to slow down and prevent, respectively, the DOPAC and HVA depletion. Neither MPTP nor EE caused changes in the gene expression of the midbrain dopaminergic system. As for cholinergic system in midbrain, MPTP induced a decrease in gene expressions of the choline acetyltransferase (ChAT) and increase of the both acetylcholinesterase (AChE) and the M1 muscarinic receptor (M1R). Using the Morris water maze, neither MPTP nor exposion to EE induced, respectively, cognitive deficits and enhancing in the reference and working memory (WM) tasks. Furthermore, no changes in gene expression of dopaminergic and cholinergic systems were reported in the prefrontal cortex. In this context, our results showed the neuroprotective potential of EE against the PD.

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