L-glutamate stimulation of Na+ efflux from brain synaptic membrane vesicles.
The characteristics of 22Na efflux from 22NaCl-preloaded synaptic plasma membrane vesicles and the stimulation of such efflux by gramicidin D and L-glutamate were determined. The rate and magnitude of passive Na+ efflux were dependent on the initial intravesicular NaCl concentration. A Na+:cation exchange process was also observed. Gramicidin D markedly enhanced Na+ efflux in a concentration-dependent manner and at 10 microM it caused total loss of intravesicular 22Na. The neuroexcitatory amino acids L-glutamate and D-glutamate, and the amino acid analog kainic acid, also stimulated Na+ efflux in a dose-dependent fashion, but their effects were weaker than those of gramicidin D. The mechanism of glutamate stimulation of Na+ flux is presumed to be through the activation of the glutamate receptor . Na+ channel complex in these membranes.
D000818:Animals; D001921:Brain / Q000378:metabolism*; D002414:Cations, Monovalent; D005971:Glutamates / Q000494:pharmacology*; D018698:Glutamic Acid; D007700:Kinetics; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000378:metabolism*; D013570:Synaptic Membranes / Q000187:drug effects / Q000378:metabolism*; D013572:Synaptic Vesicles / Q000187:drug effects / Q000378:metabolism*
D002414:Cations, Monovalent; D005971:Glutamates; D018698:Glutamic Acid; D012964:Sodium