Aromatic L-amitio acid decarboxylase in rat corpus striatum: Implications for action of L-dopa in parkinsonism

Eldad Melamed, Franz Hefti, Douglas J. Pettibone, James Liebman, Richard J. Wurtman

Research output: Contribution to journalArticlepeer-review

Abstract

We studied the distribution of aromatic L-amino acid decarboxylase (AAAD) 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 20%. 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 intemeurons 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.

Original languageEnglish
Pages (from-to)651-655
Number of pages5
JournalNeurology
Volume31
Issue number6
DOIs
StatePublished - Jun 1981
Externally publishedYes

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