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Characterization of glutamate efflux from preoptic area synaptosomes
A Fleischmann1, M H Makman, A M Etgen
1Department of Psychiatry, Albert Einstein College of Medicine, Bronx, NY 10461.
Neuropharmacology
|November 1, 1992
Summary
Ovarian steroids influence glutamate and GABA release in rats. This study shows glutamate efflux from preoptic area synaptosomes is carrier-mediated and independent of receptor activation.
Area of Science:
- Neuroscience
- Neuroendocrinology
- Neurochemistry
Background:
- Ovarian steroids impact neurotransmitter release in the preoptic area.
- Previous studies suggest a role for the glutamate carrier in steroid-modulated amino acid release.
Purpose of the Study:
- To characterize glutamate efflux and the glutamate carrier system in synaptosomes from hormone-treated ovariectomized rats.
- To investigate the mechanisms underlying glutamate efflux in the preoptic area.
Main Methods:
- Utilized [3H]glutamate efflux assays in synaptosomes from ovariectomized rats treated with ovarian steroids.
- Examined the effects of glutamate, D-aspartate, dihydrokainate, and receptor agonists/antagonists on glutamate efflux.
- Investigated the role of calcium and chloride channels in glutamate efflux.
Main Results:
- Glutamate efflux was induced by glutamate and D-aspartate, indicating carrier mediation.
- Dihydrokainate inhibited glutamate uptake but not efflux, while receptor antagonists were ineffective.
- Glutamate-induced efflux was chloride channel-dependent and did not require external calcium or receptor activation.
Conclusions:
- Glutamate efflux in the preoptic area is primarily mediated by the glutamate carrier system.
- This efflux process is independent of excitatory amino acid receptor activation.
- Ovarian steroid influence on neurotransmitter release may involve modulation of this carrier-mediated efflux pathway.