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The motor symptoms of Parkinson's disease (PD) (akinesia, rigidity, and tremor) very likely result from the progressive loss of substantia nigra pars compacta (SNpc) neurons, which produces a decreased dopamine concentration in the striatum. [1,2] This neuronal loss provokes a cascade of changes in the functioning of the basal ganglia; these changes are thought to participate in the development of this motor syndrome. Indeed, the activity of the output systems of the basal ganglia, represented by the internal segment of the pallidum (GPi) and the substantia nigra pars reticulata (SNpr), [3] is increased after nigrostriatal denervation. [4] However, although the hyperactivity of the GPi is well documented, this is not so for the activity of the SNpr. Furthermore, the SNpr differs from the GPi in terms of its (1) anatomic connections (afferent and efferent pathways) [5-7]; (2) biochemical content (methionine enkephalin and substance P) [8-10]; (3) direct contact with dendrites of the dopaminergic neurons of the SNpc, which may directly influence the activity of SNpr neurons [11,12]; and (4) involvement in the visuospatial and ocular motor function, resulting from its projection to the superior colliculus (SC), a structure related to the initiation of saccadic eye movements. [13,14]
The goals of the present study were (1) to determine whether the SNpr is hyperactive after nigrostriatal denervation and (2) to analyze the possible functional consequences of any hyperactivity of the SNpr on the SC. Because SNpr efferent neurons use gamma-aminobutyric acid (GABA) as neurotransmitter, [15,16] we analyzed the consequences of nigrostriatal denervation on GABAergic activity in the SNpr of patients with PD and its effect on tectal GABAergic neurons. Since all PD patients had received L-dopa therapy, we tested the direct effect of nigrostriatal denervation on GABAergic activity in monkeys rendered parkinsonian by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) intoxication, some received L-dopa …
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