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Striatal dopamine depletion, dopamine receptor stimulation, and GABA metabolism: Implications for the therapy of Parkinson's disease
Author(s) -
Bennett James P.
Publication year - 1986
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410190215
Subject(s) - dopamine , neurochemical , apomorphine , endocrinology , medicine , stimulation , glutamate decarboxylase , glutamate receptor , parkinson's disease , dopamine receptor d1 , dopamine receptor , chemistry , striatum , dopaminergic , neuroscience , biology , receptor , biochemistry , disease , enzyme
Dopamine‐denervated rat striata exhibit increased synaptosomal gamma‐aminobutyric acid (GABA) synthetic capacity (glutamate decarboxylase activity) without an alteration in GABA transport capacity. Stimulating denervated striatal dopamine receptors with apomorphine selectively increases in vivo steadystate striatal GABA turnover. The striatal response in animals to isolated loss of dopamine innervation is an increase in glutamate decarboxylase activity, not the decrease frequently found in the brains of patients with Parkinson's disease. Neurochemical expression of denervated striatal dopamine receptor stimulation may involve increased synaptic activity of striatal GABA neurons. For these reasons, enhancement of basal ganglia GABA function may improve responsiveness to dopamimetic therapies in patients with Parkinson's disease.