Aromatic L-Amino Acid Decarboxylase Activity of Mouse Striatum Is Modulated via Dopamine Receptors
Version of Record online: 5 OCT 2006
Journal of Neurochemistry
Volume 60, Issue 6, pages 2175–2180, June 1993
How to Cite
Hadjiconstantinou, M., Wemlinger, T. A., Sylvia, C. P., Hubble, J. P. and Neff, N. H. (1993), Aromatic L-Amino Acid Decarboxylase Activity of Mouse Striatum Is Modulated via Dopamine Receptors. Journal of Neurochemistry, 60: 2175–2180. doi: 10.1111/j.1471-4159.1993.tb03503.x
- Issue online: 5 OCT 2006
- Version of Record online: 5 OCT 2006
- Received August 25, 1992; revised manuscript received November 10, 1992; accepted November 12, 1992.
- Aromatic L-amino acid decarboxylase;
- Dopamine receptors;
- Parkinson's disease.
Abstract: Aromatic L-amino acid decarboxylase (AAAD) activity is enhanced in the striatum of control and MPTP-treated mice after administration of a single dose of the dopamine receptor antagonists haloperidol, sulpiride, and SCH 23390. MPTP-treated mice appear more sensitive to the antagonists, i.e., respond earlier and to lower doses of antagonists than control mice. The rise of AAAD activity induced by the antagonists is prevented by pretreatment with cycloheximide. The apparent Km values for L-3,4-dihydroxyphenylalanine (L-DOPA) and pyridoxal 5-phosphate appear unchanged after treatment with the antagonists. Increased AAAD activity was observed also after subchronic administration of dopamine receptor antagonists or treatment with reserpine. A single dose of a selective dopamine receptor agonists had no effect on AAAD activity. In contrast, administration of L-DOPA, quinpirole, or SKF 23390 for 7 days lowers AAAD activity in the striatum. We conclude that AAAD is modulated in striatum via dopaminergic receptors.