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The volatile anesthetic isoflurane differentially inhibits voltage-gated sodium channel currents between pyramidal and parvalbumin neurons in the prefrontal cortex
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The volatile anesthetic isoflurane differentially inhibits voltage-gated sodium channel currents between pyramidal and parvalbumin neurons in the prefrontal cortex
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Journal Article
The volatile anesthetic isoflurane differentially inhibits voltage-gated sodium channel currents between pyramidal and parvalbumin neurons in the prefrontal cortex
2023
Overview
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.
Publisher
Frontiers Research Foundation,Frontiers Media S.A
