EFFECT OF THEANINE, R-GLUTAMYLETHYLAMIDE, ON BRAIN MONOAMINES AND STRIATAL DOPAMINE RELEASE IN CONSCIOUS RATS

Citation
H. Yokogoshi et al., EFFECT OF THEANINE, R-GLUTAMYLETHYLAMIDE, ON BRAIN MONOAMINES AND STRIATAL DOPAMINE RELEASE IN CONSCIOUS RATS, Neurochemical research, 23(5), 1998, pp. 667-673
Citations number
29
Categorie Soggetti
Biology,Neurosciences
Journal title
ISSN journal
03643190
Volume
23
Issue
5
Year of publication
1998
Pages
667 - 673
Database
ISI
SICI code
0364-3190(1998)23:5<667:EOTROB>2.0.ZU;2-C
Abstract
Theanine, r-glutamylethylamide, is one of the major components of amin o acids in Japanese green tea. Effect of theanine on brain amino acids and monoamines, and the striatal release of dopamine (DA) was investi gated. Determination of amino acids in the brain after the intragastri c administration of theanine showed that theanine was incorporated int o brain through blood-brain barrier via leucine-preferring transport s ystem. The concentrations of norepinephrine, 3,4-dihydroxyphenylacetic acid (DOPAC) and 5-hydroxyindole acetic acid (5HIAA) in the brain reg ions were unaffected by the theanine administration except in striatum . Theanine administration caused significant increases in serotonin an d/or DA concentrations in the brain, especially in striatum, hypothala mus and hippocampus. Direct administration of theanine into brain stri atum by microinjection caused a significant increase of DA release in a dose-dependent manner. Microdialysis of brain with calcium-free Ring er buffer attenuated the theanine-induced DA release. Pretreatment wit h the Ringer buffer containing an antagonist of non-NMDA (N-methyl-D-a spartate) glutamate receptor, MK-801, for 1 hr did not change the sign ificant increase of DA release induced by theanine. However, in the ca se of pretreatment with AP-5, (+/-)-2-amino-5-phosphonopentanoic acid; antagonist of NMDA glutamate receptor, the theanine-induced DA releas e from striatum was significantly inhibited. These results suggest tha t theanine might affect the metabolism and/or the release of some neur otransmitters in the brain, such as DA.