Effects of glutamate antagonists on the activity of aromatic L-amino acid decarboxylase
Autor: | M. S. Starr, C. S. Biggs, A. Fisher |
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Rok vydání: | 1999 |
Předmět: |
Clinical Biochemistry
Glutamate decarboxylase AMPA receptor Budipine Pharmacology Biochemistry Receptors N-Methyl-D-Aspartate chemistry.chemical_compound medicine Animals Aromatic Amino Acid Decarboxylase Inhibitors Receptors AMPA Rats Wistar Organic Chemistry Memantine Corpus Striatum Rats Enzyme Activation nervous system chemistry Competitive antagonist Aromatic-L-Amino-Acid Decarboxylases NMDA receptor NBQX Excitatory Amino Acid Antagonists Eliprodil medicine.drug |
Zdroj: | Amino acids. 14(1-3) |
ISSN: | 0939-4451 |
Popis: | This study examines the hypothesis that glutamate tonically suppresses the activity of the enzyme aromatic L-amino acid decarboxylase (AADC), and hence the biosynthesis of dopamine, to explain how antagonists of glutamate receptors might potentiale the motor actions of L-DOPA in animal models of Parkinson's disease. A variety of glutamate antagonists were therefore administered acutely to normal rats, which were sacrificed 30–60 min later and AADC activity assayed in the substantia nigra pars reticulate (SNr) and corpus striatum (CS). The NMDA receptor-ion channel antagonists MK 801, budipine, amantadine, memantine and dextromethorphan all caused a pronounced in creased in AADC activity, more especially in the SNr than CS. The NMDA glycine site antagonist (R)-HA 966 produced a modest increase in AADC activity in the CS but not SNr, whilst the NMDA polyamine site antagonist eliprodil, the NMDA competitive antagonist CGP 40116 and the AMPA antagonist NBQX were without effect. The results suggest that an increase in dopamine synthesis might contribute to the L-DOPA-facilitating actions of some glutamate antagonists. |
Databáze: | OpenAIRE |
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