| Autor: |
Michaelis, Elias, Magruder, Charles, Lampe, Richard, Galton, Noemi, Chang, Hsuan, Michaelis, Mary |
| Zdroj: |
Neurochemical Research; Jan1984, Vol. 9 Issue 1, p29-44, 16p |
| Abstrakt: |
Four amphipathic molecules with known local anesthetic activity, dibucaine, tetracaine, chlorpomazine, and quinacrine, inhibited the binding of l-[H]glutamic acid to rat brain synaptic plasma membranes and to the purified glutamate binding protein. Neither haloperidol nor diphenylhydantoin had significant inhibitory effects on the glutamate binding activity of the membranes or of the purified protein. The amphipathic drugs apparently inhibited l-[H]glutamate binding to synaptic membranes by a mixed type of inhibition. The inhibitory activity of quinacrine on glutamate binding to the synaptic membranes was greater in a low ionic strength, Ca-free buffer medium, than in a physiologic medium (Krebs-Henseleit buffer). Removal of Ca from the Krebs solution enhanced quinacrine's inhibition of glutamate binding. Quinacrine up to 1 mM concentration did not inhibit the high affinity Na-dependent l-glutamate transport in these membrane preparations. The importance of Ca in the expression of quinacrine's effects on the glutamate binding activity of synaptic membranes and the observed tetracaine and chlorpromazine-induced increases in the transition temperature for the glutamate binding process of these membranes, were indicative of an interaction of the local anesthetics with the lipid environment of the glutamate binding sites. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
|
Full text from SpringerLink