Effect of propofol on glutamate and gamma-aminobutyric acid release from rat hippocampal synaptosomes.
- Author:
You, SHANG
;
Shanglong, YAO
;
Yinming, ZENG
;
Hongliang, LIU
;
Junli, CAO
- Publication Type:Journal Article
- MeSH:
Anesthetics, Intravenous/pharmacology;
Calcium/metabolism;
Glutamic Acid/*biosynthesis;
Hippocampus/*metabolism;
Propofol/*pharmacology;
Rats, Sprague-Dawley;
Synaptosomes/*metabolism;
gamma-Aminobutyric Acid/*biosynthesis
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2005;25(6):700-2
- CountryChina
- Language:English
-
Abstract:
To investigate the effect of propofol on the release of glutamate and gamma-aminobutyric acid (GABA) from rat hippocampal synatosomes, synaptosomes was made from hippocampus and incubated with artificial cerebrospinal fluid (aCSF). With the experiment of Ca(2+)-dependent release of glutamate and GABA, dihydrokainic acid (DHK) and nipectic acid were added into aCSF. For the observation of Ca(2+)-independent release of glutamate and GABA, no DHK, nipectic acid and Ca2+ were added from aCSF. The release of glutamate and GABA were evoked by 20 micromol/L veratridine or 30 mmol/L KCI. The concentration of glutamate and GABA in aCSF was measured by using high-performance liquid chromatography (HPLC). 30, 100 and 300 micromol/L propofol significantly inhibited veratridine-evoked Ca(2+)-dependent release of glutamate and GABA (P < 0.01 or P < 0. 05). However, propofol showed no effect on elevated KCl-evoked Ca(2+)-dependent release of glutamate and GABA (P > 0.05). Veratridine or elevated KCI evoked Ca(2+)-independent release of glutamate and GABA was not affected significantly by propofol (P > 0.05). Propofol could inhibit Ca(2+)-dependent release of glutamate and GABA. However, it has no effect on the Ca(2+)-independent release of glutamate and GABA.
