Cortical lesions modulate turnover rates of acetylcholine and gamma-aminobutyric acid.

Interruption of the cortico-striatal glutamatergic pathway by decoratication results in significant decreases in the turnover rates of acetylcholine TRACh and gamma-aminobutyric acid TRGABA of striatum. These data support the hypothesis that the cortical input to the striatum is excitatory and acts to modulate cholinergic and GABAergic function in this nucleus. Studies of kainate-induced lesions of the striatum also indicate that most striatal cholinergic interneurons receive a glutamatergic input and that multiple injections of kainate are required to destroy this large population of interneurons.