The volatile anesthetic isoflurane differentially inhibits voltage-gated sodium channel currents between pyramidal and parvalbumin neurons in the prefrontal cortex

How volatile anesthetics work remains poorly understood. Modulations of synaptic neurotransmission are the direct cellular mechanisms of volatile anesthetics in the central nervous system. Volatile anesthetics such as isoflurane may reduce neuronal interaction by differentially inhibiting neurotrans...

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Vydáno v:Frontiers in neural circuits Ročník 17; s. 1185095
Hlavní autoři: Qiu, Jingxuan, Yang, Yaoxin, Liu, Jin, Zhao, Wenling, Li, Qian, Zhu, Tao, Liang, Peng, Zhou, Cheng
Médium: Journal Article
Jazyk:angličtina
Vydáno: Switzerland Frontiers Research Foundation 16.06.2023
Frontiers Media S.A
Témata:
Anesthetics
Anesthetics, Inhalation - pharmacology
Animals
Brain
Brain slice preparation
Central nervous system
Cerebrospinal fluid
Channel gating
cortex
Electrophysiological recording
Exocytosis
Glutamatergic transmission
Isoflurane
Isoflurane - pharmacology
Laboratories
Mice
Neurons
Neuroscience
Neurotransmission
Parvalbumin
parvalbumin neurons
Parvalbumins
Prefrontal Cortex
Pyramidal cells
Pyramidal Cells - physiology
pyramidal neurons
Simulation
Sodium channels (voltage-gated)
Software
Unconsciousness
voltage-gated sodium channel (Nav)
Voltage-Gated Sodium Channels
γ-Aminobutyric acid
United States > US
China
cortex
pyramidal neurons
voltage-gated sodium channel (Nav)
isoflurane
parvalbumin neurons
ISSN:1662-5110, 1662-5110
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Shrnutí:How volatile anesthetics work remains poorly understood. Modulations of synaptic neurotransmission are the direct cellular mechanisms of volatile anesthetics in the central nervous system. Volatile anesthetics such as isoflurane may reduce neuronal interaction by differentially inhibiting neurotransmission between GABAergic and glutamatergic synapses. Presynaptic voltage-dependent sodium channels (Na ), which are strictly coupled with synaptic vesicle exocytosis, are inhibited by volatile anesthetics and may contribute to the selectivity of isoflurane between GABAergic and glutamatergic synapses. However, it is still unknown how isoflurane at clinical concentrations differentially modulates Na currents between excitatory and inhibitory neurons at the tissue level. In this study, an electrophysiological recording was applied in cortex slices to investigate the effects of isoflurane on Na between parvalbumin (PV ) and pyramidal neurons in PV-cre-tdTomato and/or vglut2-cre-tdTomato mice. Isoflurane at clinically relevant concentrations produced a hyperpolarizing shift in the voltage-dependent inactivation and slowed the recovery time from the fast inactivation in both cellular subtypes. Since the voltage of half-maximal inactivation was significantly depolarized in PV neurons compared to that of pyramidal neurons, isoflurane inhibited the peak Na currents in pyramidal neurons more potently than those of PV neurons (35.95 ± 13.32% vs. 19.24 ± 16.04%, = 0.036 by the Mann-Whitney test). Isoflurane differentially inhibits Na currents between pyramidal and PV neurons in the prefrontal cortex, which may contribute to the preferential suppression of glutamate release over GABA release, resulting in the net depression of excitatory-inhibitory circuits in the prefrontal cortex.
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These authors have contributed equally to this work
Edited by: Qian-Quan Sun, University of Wyoming, United States
Reviewed by: Jiaman Dai, University of Wyoming, United States; Hiroshi Onimaru, Showa University, Japan; Liang Zhang, University of Toronto, Canada
ISSN:1662-5110
1662-5110
DOI:10.3389/fncir.2023.1185095