Evidence map›Paper›PMID 31166240›Full record

ArticleAnesthesiology2019

Isoflurane Modulates Hippocampal Cornu Ammonis Pyramidal Neuron Excitability by Inhibition of Both Transient and Persistent Sodium Currents in Mice.

Wenling Zhao, Mingyue Zhang, Jin Liu, Peng Liang, Rurong Wang, Hugh C Hemmings, Cheng Zhou

Open access · bronzeAbstract read
In one paragraph

Article in Anesthesiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  7. Poly-dipeptides produced fromProceedings of the National Academy of Sciences of the United States of America · 2022
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  8. A hypothesis concerning distinct schemes of olfactory activation evoked by perceived versus nonperceived input.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 2 countries.

Wenling ZhaoFrom the Laboratory of Anesthesia and Critical Care Medicine, Translational Neuroscience Center (W.Z., M.Z., J.L., C.Z.) Department of Anesthesiology (W.Z., M.Z., J.L., P.L., R.W., C.Z.), West China Hospital of Sichuan University, Chengdu, Sichuan, China Departments of Anesthesiology and Pharmacology, Weill Cornell Medicine, New York, New York (H.C.H.).
Mingyue Zhang
Jin Liu
Peng Liang
Rurong Wang
Hugh C Hemmings
Cheng Zhou
Cornell University · US

Funding

SYNAPTIC MECHANISMS OF GENERAL ANESTHETIC ACTIONR01GM058055 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI HEMMINGS, HUGH C · 1998 to 2023
$10.1M
NIGMS NIH HHS R01 GM058055
6 · The paper itself

Abstract

backgroundVolatile anesthetics inhibit presynaptic voltage-gated sodium channels to reduce neurotransmitter release, but their effects on excitatory neuron excitability by sodium current inhibition are unclear. The authors hypothesized that inhibition of transient and persistent neuronal sodium currents by the volatile anesthetic isoflurane contributes to reduced hippocampal pyramidal neuron excitability.

methodsWhole-cell patch-clamp recordings of sodium currents of hippocampal cornu ammonis pyramidal neurons were performed in acute mouse brain slices. The actions of isoflurane on both transient and persistent sodium currents were analyzed at clinically relevant concentrations of isoflurane.

resultsThe median inhibitory concentration of isoflurane for inhibition of transient sodium currents was 1.0 ± 0.3 mM (~3.7 minimum alveolar concentration [MAC]) from a physiologic holding potential of -70 mV. Currents from a hyperpolarized holding potential of -120 mV were minimally inhibited (median inhibitory concentration = 3.6 ± 0.7 mM, ~13.3 MAC). Isoflurane (0.55 mM; ~2 MAC) shifted the voltage-dependence of steady-state inactivation by -6.5 ± 1.0 mV (n = 11, P < 0.0001), but did not affect the voltage-dependence of activation. Isoflurane increased the time constant for sodium channel recovery from 7.5 ± 0.6 to 12.7 ± 1.3 ms (n = 13, P < 0.001). Isoflurane also reduced persistent sodium current density (median inhibitory concentration = 0.4 ± 0.1 mM, ~1.5 MAC) and resurgent currents. Isoflurane (0.55 mM; ~2 MAC) reduced action potential amplitude, and hyperpolarized resting membrane potential from -54.6 ± 2.3 to -58.7 ± 2.1 mV (n = 16, P = 0.001).

conclusionsIsoflurane at clinically relevant concentrations inhibits both transient and persistent sodium currents in hippocampal cornu ammonis pyramidal neurons. These mechanisms may contribute to reductions in both hippocampal neuron excitability and synaptic neurotransmission.

Indexed as

Action PotentialsAnesthetics, InhalationAnimalsFemaleHippocampusIsofluraneMaleMiceModels, AnimalPyramidal CellsSodium ChannelsAnesthetics, InhalationIsofluraneSodium Channels

Identifiers

PMID31166240
PMCPMC6586485
OpenAlexW2951240703

What OpenQuestion holds

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Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.