We measured the concentration of
gamma-aminobutyric acid (
GABA),
glutamic acid, and o-
phosphoethanolamine in autopsied brain of 9 patients who died with
idiopathic Parkinson's disease and 10 control subjects. In the control striatum
GABA showed an uneven rostrocaudal distribution pattern with rostral subdivisions containing about 40 to 50% higher levels. When compared with controls,
GABA concentrations in
Parkinson's disease striatum were generally elevated. The
GABA elevation was most pronounced in the caudal subdivision of the putamen; this striatal subdivision also showed the most severe
dopamine loss. We observed in the caudal putamen a significant negative correlation between the (elevated)
GABA and (reduced)
dopamine levels (the latter expressed as the sum of
dopamine plus 3-
methoxytyramine). Milder nonsignificant elevations of
GABA levels were observed in intermediate and rostral putamen followed by the caudate head subdivisions.
GABA levels were normal in all extrastriatal brain areas examined. Striatal
glutamic acid levels were markedly elevated in 3 of the 9 patients with
Parkinson's disease. We suggest that the altered
GABA metabolism in the striatum, especially the putamen, is consequent to the nigrostriatal deficiency in this disorder. This secondary change in striatal
GABA function is likely to contribute to the basal ganglia dysfunction produced by the striatal
dopamine loss and thus may be related to certain aspects of parkinsonian symptomatology.