Cholinergic synaptic transmissions were altered after single sevoflurane exposure in Drosophila pupa.

Rongfa Chen,Zhen Chen,Liting Kuang,Yang Niu,Tao Zhang,Kangqing Xu,Dongzhi Ran,Huaiyu Gu

doi:10.1155/2015/485709

Abstract

Purpose. Sevoflurane, one of the most used general anesthetics, is widely used in clinical practice all over the world. Previous studies indicated that sevoflurane could induce neuron apoptosis and neural deficit causing query in the safety of anesthesia using sevoflurane. The present study was designed to investigate the effects of sevoflurane on electrophysiology in Drosophila pupa whose excitatory neurotransmitter is acetylcholine early after sevoflurane exposure using whole brain recording technique. Methods. Wide types of Drosophila (canton-s flies) were allocated to control and sevoflurane groups randomly. Sevoflurane groups (1% sevoflurane; 2% sevoflurane; 3% sevoflurane) were exposed to sevoflurane and the exposure lasted 5 hours, respectively. All flies were subjected to electrophysiology experiment using patch clamp 24 hours after exposure. Results. The results showed that, 24 hours after sevoflurane exposure, frequency but not the amplitude of miniature excitatory postsynaptic currents (mEPSCs) was significantly reduced (P < 0.05). Furthermore, we explored the underlying mechanism and found that calcium currents density, which partially regulated the frequency of mEPSCs, was significantly reduced after sevoflurane exposure (P < 0.05). Conclusions. All these suggested that sevoflurane could alter the mEPSCs that are related to synaptic plasticity partially through modulating calcium channel early after sevoflurane exposure.

Highlights

Sevoflurane, an ether inhalational general anesthetic, with its low pungency, nonirritating odor, and low blood/gas partition coefficient, has been widely used in clinical anesthesia [1]
Since there is much advancement in surgery recently incidence and duration of exposure to sevoflurane in people receiving surgery are increasing. These raised concerns that whether anesthesia using sevoflurane would contribute to postoperative cognitive dysfunction (POCD) as rodent studies indicated that persistent learning deficit and social behavior dysfunction occurred after general anesthesia [2, 3]
projection neurons (PNs) are members of the synaptic net in which fast excitatory synaptic transmission was mediated by the α-bungarotoxin- (α-BTX-) sensitive nicotinic acetylcholine receptors

Summary

Introduction

Sevoflurane, an ether inhalational general anesthetic, with its low pungency, nonirritating odor, and low blood/gas partition coefficient, has been widely used in clinical anesthesia [1]. Since there is much advancement in surgery recently incidence and duration of exposure to sevoflurane in people receiving surgery are increasing These raised concerns that whether anesthesia using sevoflurane would contribute to postoperative cognitive dysfunction (POCD) as rodent studies indicated that persistent learning deficit and social behavior dysfunction occurred after general anesthesia [2, 3]. Previous studies indicated that isoflurane, thiopental, propofol, and ketamine would cause neurodegeneration and learning and memory deficiency [4, 5] These suggested that the neurotoxicity induced by inhalational anesthetic might be mediated by activation of γ-aminobutyric acid (GABA) and inhibition of N-methyl-D-aspartic acid (NMDA) receptor [5,6,7]

Methods

Results

Discussion

Conclusion