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Study of the Neuropeptide Function in Parkinson’s Disease Using the 6-Hydroxydopamine Model of Experimental Hemiparkinsonism

1 Unit of Physiology, University of Jaén, 23071 Jaén, Spain;
2 Cardiovascular and Metabolic Syndrome Adviser, 2842 Rossemaison, Switzerland

Parkinson’s disease, one of the most common neurodegenerative diseases, characterized by unilateral brain dopamine damage in its initial stages, remains unknown in many respects. It is especially necessary to improve the early diagnosis and, in order to improve the treatment, to go thoroughly into the knowledge of its pathophysiology. To do this, it is essential to perform studies in appropriate animal models of the disease. One of those is generated by the unilateral intracerebral administration of the neurotoxic 6-hydroxydopamine that produces clear asymmetrical cerebral dopamine depletion. Currently the neuronal coexistence of several neurotransmitters is obvious. Particularly interesting is the coexistence of dopamine with various neuropeptides. If the neuronal content of dopamine is asymmetrically altered in the early stages of the Parkinson’s disease, the coexisting neuropeptides may also be asymmetrically altered. Therefore, their study is important to appropriately understand the pathogenesis of the Parkinson’s disease. The function of the neuropeptides can be studied through their metabolism by neuropeptidases whose activity reflects the functional status of their endogenous substrates as well as the one of the peptides resulting from their hydrolysis. Here we review the 6-hydroxydopamine model of experimental hemiparkinsonism as an appropriate model to study the initial asymmetric stages of the disease. In particular, we analyze the consequences of unilateral brain dopamine depletions on the functionality of brain neuropeptides through the study of the activity of cerebral neuropeptidases.
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