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Amantadine increases aromatic 1L‐amino acid decarboxylase mRNA in PC12 cells
Author(s) -
Li XinMin,
Juorio Augusto V.,
Qi Jin,
Boulton Alan A.
Publication year - 1998
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19980815)53:4<490::aid-jnr11>3.0.co;2-6
Subject(s) - amantadine , aromatic l amino acid decarboxylase , parkinsonism , dopamine , pharmacology , levodopa , chemistry , benserazide , decarboxylation , stimulation , messenger rna , medicine , endocrinology , biology , parkinson's disease , biochemistry , gene , disease , catalysis
Amantadine is an antiviral agent that was unexpectedly found to cause symptomatic improvement in patients with Parkinsonism, although its mechanism of action remains to be elucidated. Aromatic L‐amino acid decarboxylase (AADC) is a regulated enzyme that catalyzes the decarboxylation of 3,4‐dihydroxyphenylalanine (L‐Dopa). It may be especially important during L‐Dopa therapy in Parkinsonism, during which it may be rate‐limiting for the production of dopamine. This study reports the effects of amantadine on the gene expression of AADC in PC12 cells. It shows that amantadine induces AADC gene expression at concentrations of 10 and 100 μM after 24 hr of incubation. The results suggest that the stimulation of AADC mRNA by amantadine may be one of its effects on dopamine metabolism that may have relevance for potentiation of L‐Dopa therapy in Parkinsonism. J. Neurosci. Res. 53:490–493, 1998. © 1998 Wiley‐Liss, Inc.