The roles of protein tyrosine kinase at glutamate-induced Ca2+ entry in primary cultured corticocerebral neurons
- Author:
Jian LIANG
1
Author Information
1. Dept. of Pharmacology, Sun Yat-Sen Univ. of Med. Sciences
- Publication Type:Journal Article
- Keywords:
Ca2+ channel;
Glutamate;
Neurons;
Protein tyrosine kinase
- From:
Chinese Pharmacological Bulletin
2002;18(2):152-155
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To investigate effects of genistein, an inhibitor of protein tyrosine kinase and vanadate, the inhibitor of protein tyrosine phophorylation, on glutamate-induced Ca2+ entry in rat primary cultured corticocerebral neurons. METHODS: The effects of drug on cytoplasmic Ca2+ level ([Ca2+]i) were invesgated with Fura-2/AM fluorescence technique. RESULTS The increase in [Ca2+]i induced by glutamate was significantly reduced by genistein (from 1 to 30 μmol·L-1) and NMDA receptor antagonist MK-801 (1 μmol·L-1), not by nimodipine (1 μmol·L-1) and SK&F96365. Vanadate (from 1 to 30 μmol·L-1) significantly enhanced glutamine-induced [Ca2+]i response. CONCLUSION: Nimdipine-sensitive Ca2+ channel and SK&F96365-sensitive Ca2+ channels are not related to glutamate-induced Ca2+ entry. It is related to the activation of protein tyrosine kinase in rat primary cultured corticocerebral neurons.
