The basal ganglia are a group of brain structures involved in the control of motor and psychoaffective behaviors. Unfortunately, those structures are the targets of devastating neurodegenerative diseases such as Parkinson's disease and Huntington's chorea. Parkinson's disease is characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta. The loss of those dopaminergic neurons leads to an imbalance of activity in the other components of the basal ganglia which, eventually, results in movement deficits such as akinesia, rigidity and tremor. Although the etiology of Parkinson's disease remains to be established, evidence indicates that excitotoxicity somehow participates in the death of midbrain dopaminergic neurons. A prerequisite to this hypothesis is that dopaminergic neurons receive glutamatergic afferents and express calcium-permeable glutamate receptors. During the past year, we demonstrated that such is, indeed, the case in monkeys. Moreover, we demonstrated that the density of glutamatergic innervation and the level of expression of glutamate receptors is highly variable among the different populations of midbrain dopaminergic neurons which, in fact, do not show the same pattern of degeneration in Parkinson's disease. These results were presented in abstract form at major scientific meetings and have been published in peer-reviewed journals. A better understanding of the mechanism underlying the death of midbrain dopaminergic neurons in Parkinson's disease will help to develop therapies to control, and even prevent, the degenerative process.
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