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Aromatic L-amino acid decarboxylase in rat corpus striatum

Implications for action of L-dopa in parkinsonism

From the Laboratory of Neuroendocrine Regulation, Department of Nutrition and Food Science, Massachusetts Institute of Technology, Cambridge, MA.

We studied the distribution of aromatic L-amino acid decarboxylase (UD) activity in striatal compartments of rats. After near-total destruction of nigrostriatal dopaminergic neurons, 15 to 20% of the initial enzyme activity remained. Striatal enzyme activity remained unchanged after destruction of serotoninergic terminals by electrolytic raphe lesions. Combined raphe-nigrostriatal lesions or nigrostriatal lesions alone produced similar decreases in striatal decarboxylase. Intrastriatal injection of kainic acid (which selectively destroys striatal interneurons and efferent neurons and also induces marked glial proliferation) reduced activity by 200/0. Only 7% of initial striatal activity (perhaps localized in capillaries) remained after combined nigrostriatal-kainic acid lesions. These findings indicate that after degeneration of dopaminergic terminals, striatal interneurons and efferent neurons, but not serotonergic terminals or glia, contain an important fraction of the residual AAAD. This compartment may be the site of enzymatic conversion of exogenous L-dopa to dopamine in the parkinsonian striatum.

Address correspondence and reprint requests to Dr. Wurtman, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139.

This work was supported in part by the National Institutes of Health and by the American Parkinson's Disease Association.

Presented in part at the thirty-second annual meeting of the American Academy of Neurology, New Orleans, LA, May 1980.

Accepted for publication September 23, 1980.

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