Inhibitory effects of propofol on excitatory synaptic transmission in supraoptic nucleus neurons in vitro.
- Author:
Huan-Huan ZHANG
1
;
Chao ZHENG
1
;
Bang-An WANG
1
;
Meng-Ya WANG
2
Author Information
1. Cell Electrophysiology Laboratory, Wannan Medical College, Wuhu 241002, China.
2. Cell Electrophysiology Laboratory, Wannan Medical College, Wuhu 241002, China. wangmy@wnmc.edu.cn.
- Publication Type:Journal Article
- MeSH:
Anesthetics, Intravenous;
pharmacology;
Animals;
Excitatory Postsynaptic Potentials;
drug effects;
GABA-A Receptor Antagonists;
pharmacology;
Glutamic Acid;
pharmacology;
In Vitro Techniques;
Neurons;
drug effects;
Propofol;
pharmacology;
Rats;
Receptors, Glutamate;
metabolism;
Supraoptic Nucleus;
cytology
- From:
Acta Physiologica Sinica
2015;67(6):583-590
- CountryChina
- Language:English
-
Abstract:
The present study was designed to investigate the inhibitory effects of intravenous general anesthetic propofol (0.1-3.0 mmol/L) on excitatory synaptic transmission in supraoptic nucleus (SON) neurons of rats, and to explore the underlying mechanisms by using intracellular recording technique and hypothalamic slice preparation. It was observed that stimulation of the dorsolateral region of SON could elicit the postsynaptic potentials (PSPs) in SON neurons. Of the 8 tested SON neurons, the PSPs of 7 (88%, 7/8) neurons were decreased by propofol in a concentration-dependent manner, in terms of the PSPs' amplitude (P < 0.01), area under curve, duration, half-width and 10%-90% decay time (P < 0.05). The PSPs were completely and reversibly abolished by 1.0 mmol/L propofol at 2 out of 7 tested cells. The depolarization responses induced by pressure ejection of exogenous glutamate were reversibly and concentration-dependently decreased by bath application of propofol. The PSPs and glutamate-induced responses recorded simultaneously were reversibly and concentration-dependently decreased by propofol, but 0.3 mmol/L propofol only abolished PSPs. The excitatory postsynaptic potentials (EPSPs) of 7 cells increased in the condition of picrotoxin (30 µmol/L, a GABA(A) receptor antagonist) pretreatment. On this basis, the inhibitory effects of propofol on EPSPs were decreased. These data indicate that the presynaptic and postsynaptic mechanisms may be both involved in the inhibitory effects of propofol on excitatory synaptic transmission in SON neurons. The inhibitory effects of propofol on excitatory synaptic transmission of SON neurons may be related to the activation of GABA(A) receptors, but at a high concentration, propofol may also act directly on glutamate receptors.
