Cholinergic Synaptic Transmissions Were Altered after Single Sevoflurane Exposure inDrosophilaPupa

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.

Update on the Mechanism and Treatment of Sevoflurane-Induced Postoperative Cognitive Dysfunction

“…Sevoflurane has a wide range of effects on voltage-dependent ion channels ( Yokoyama et al, 2011 ; Liu Y. et al, 2016 ; Fukushima et al, 2020 ). Chen et al (2015) suggested that exposure to sevoflurane could reduce the transmission of cholinergic synapses by inhibiting the Ca 2+ current. Furthermore, Silva et al (2005) proposed that sevoflurane could promote the release of ACh in the cerebral cortex of rats by releasing Ca 2+ .…”

The Mechanisms of Sevoflurane-Induced Neuroinflammation

“…It has been reported that the clinical concentration of sevoflurane can inhibit ACh release in a dose-dependent manner (Shichino et al, 1998). Furthermore, an experiment by Chen et al (2015) in Drosophila melanogaster showed that 1, 2, and 3% sevoflurane for 24 h reduced presynaptic cholinergic neurotransmission, partially by inhibiting calcium current. Interestingly, the in vitro study by Naruo et al (2005) demonstrated that a clinically relevant sevoflurane concentration (i.e., 0.5-3%) inhibited the postsynaptic cholinergic neurotransmitters without the influence of presynaptic exocytosis or endocytosis, which instead functioned by nAChR blocking on the postsynaptic neuron.…”

IL-17A deletion reduces sevoflurane-induced neurocognitive impairment in neonatal mice by inhibiting NF-κB signaling pathway

“…Although the mechanism of neurotoxicity of sevoflurane is not completely clear, many studies have shown that the pathogenesis of sevoflurane-induced cognitive impairment may be related to neuroinflammation [ 6–8 ]. Recent studies have suggested that sevoflurane causes neuroinflammation by activating microglia [ 9 ] and peripheral immune cells, destroying the permeability of the blood–brain barrier [ 10 ], decreasing gut microbiota [ 11 ] and modulating cholinergic synaptic transmission, which can lead to cognitive impairment [ 12 ]. The hippocampus, a center for learning and memory, robustly expresses IL-1β receptor, which play key roles in learning and memory as pro-inflammatory factor receptors.…”