Phospholipase C-related inactive protein type-1 deficiency affects anesthetic electroencephalogram activity induced by propofol and etomidate in mice

Tomonori Furukawa, Yoshikazu Nikaido, Shuji Shimoyama, Yoshiki Ogata, Tetsuya Kushikata, Kazuyoshi Hirota, Takashi Kanematsu, Masato Hirata, Shinya Ueno

Research output: Contribution to journalArticle

Abstract

Purpose: The general anesthetics propofol and etomidate mainly exert their anesthetic actions via GABA A receptor (GABAA-R). The GABAA-R activity is influenced by phospholipase C-related inactive protein type-1 (PRIP-1), which is related to trafficking and subcellular localization of GABAA-R. PRIP-1 deficiency attenuates the behavioral reactions to propofol but not etomidate. However, the effect of these anesthetics and of PRIP-1 deficiency on brain activity of CNS are still unclear. In this study, we examined the effects of propofol and etomidate on the electroencephalogram (EEG). Methods: The cortical EEG activity was recorded in wild-type (WT) and PRIP-1 knockout (PRIP-1 KO) mice. All recorded EEG data were offline analyzed, and the power spectral density and 95% spectral edge frequency of EEG signals were compared between genotypes before and after injections of anesthetics. Results: PRIP-1 deficiency induced increases in EEG absolute powers, but did not markedly change the relative spectral powers during waking and sleep states in the absence of anesthesia. Propofol administration induced increases in low-frequency relative EEG activity and decreases in SEF95 values in WT but not in PRIP-1 KO mice. Following etomidate injection, low-frequency EEG power was increased in both genotype groups. At high frequency, the relative power in PRIP-1 KO mice was smaller than that in WT mice. Conclusions: The lack of PRIP-1 disrupted the EEG power distribution, but did not affect the depth of anesthesia after etomidate administration. Our analyses suggest that PRIP-1 is differentially involved in anesthetic EEG activity with the regulation of GABAA-R activity.

Original languageEnglish
Pages (from-to)531-542
Number of pages12
JournalJournal of Anesthesia
Volume33
Issue number4
DOIs
Publication statusPublished - Aug 20 2019

Fingerprint

Etomidate
Protein Deficiency
Type C Phospholipases
Propofol
Anesthetics
Electroencephalography
GABA-A Receptors
Proteins
Anesthesia
Genotype
General Anesthetics
Injections
Knockout Mice
Sleep

All Science Journal Classification (ASJC) codes

  • Anesthesiology and Pain Medicine

Cite this

Phospholipase C-related inactive protein type-1 deficiency affects anesthetic electroencephalogram activity induced by propofol and etomidate in mice. / Furukawa, Tomonori; Nikaido, Yoshikazu; Shimoyama, Shuji; Ogata, Yoshiki; Kushikata, Tetsuya; Hirota, Kazuyoshi; Kanematsu, Takashi; Hirata, Masato; Ueno, Shinya.

In: Journal of Anesthesia, Vol. 33, No. 4, 20.08.2019, p. 531-542.

Research output: Contribution to journalArticle

Furukawa, Tomonori ; Nikaido, Yoshikazu ; Shimoyama, Shuji ; Ogata, Yoshiki ; Kushikata, Tetsuya ; Hirota, Kazuyoshi ; Kanematsu, Takashi ; Hirata, Masato ; Ueno, Shinya. / Phospholipase C-related inactive protein type-1 deficiency affects anesthetic electroencephalogram activity induced by propofol and etomidate in mice. In: Journal of Anesthesia. 2019 ; Vol. 33, No. 4. pp. 531-542.
@article{b5b45d38633e42e99ecb165c326bd8e8,
title = "Phospholipase C-related inactive protein type-1 deficiency affects anesthetic electroencephalogram activity induced by propofol and etomidate in mice",
abstract = "Purpose: The general anesthetics propofol and etomidate mainly exert their anesthetic actions via GABA A receptor (GABAA-R). The GABAA-R activity is influenced by phospholipase C-related inactive protein type-1 (PRIP-1), which is related to trafficking and subcellular localization of GABAA-R. PRIP-1 deficiency attenuates the behavioral reactions to propofol but not etomidate. However, the effect of these anesthetics and of PRIP-1 deficiency on brain activity of CNS are still unclear. In this study, we examined the effects of propofol and etomidate on the electroencephalogram (EEG). Methods: The cortical EEG activity was recorded in wild-type (WT) and PRIP-1 knockout (PRIP-1 KO) mice. All recorded EEG data were offline analyzed, and the power spectral density and 95{\%} spectral edge frequency of EEG signals were compared between genotypes before and after injections of anesthetics. Results: PRIP-1 deficiency induced increases in EEG absolute powers, but did not markedly change the relative spectral powers during waking and sleep states in the absence of anesthesia. Propofol administration induced increases in low-frequency relative EEG activity and decreases in SEF95 values in WT but not in PRIP-1 KO mice. Following etomidate injection, low-frequency EEG power was increased in both genotype groups. At high frequency, the relative power in PRIP-1 KO mice was smaller than that in WT mice. Conclusions: The lack of PRIP-1 disrupted the EEG power distribution, but did not affect the depth of anesthesia after etomidate administration. Our analyses suggest that PRIP-1 is differentially involved in anesthetic EEG activity with the regulation of GABAA-R activity.",
author = "Tomonori Furukawa and Yoshikazu Nikaido and Shuji Shimoyama and Yoshiki Ogata and Tetsuya Kushikata and Kazuyoshi Hirota and Takashi Kanematsu and Masato Hirata and Shinya Ueno",
year = "2019",
month = "8",
day = "20",
doi = "10.1007/s00540-019-02663-z",
language = "English",
volume = "33",
pages = "531--542",
journal = "Journal of Anesthesia",
issn = "0913-8668",
publisher = "Springer Japan",
number = "4",

}

TY - JOUR

T1 - Phospholipase C-related inactive protein type-1 deficiency affects anesthetic electroencephalogram activity induced by propofol and etomidate in mice

AU - Furukawa, Tomonori

AU - Nikaido, Yoshikazu

AU - Shimoyama, Shuji

AU - Ogata, Yoshiki

AU - Kushikata, Tetsuya

AU - Hirota, Kazuyoshi

AU - Kanematsu, Takashi

AU - Hirata, Masato

AU - Ueno, Shinya

PY - 2019/8/20

Y1 - 2019/8/20

N2 - Purpose: The general anesthetics propofol and etomidate mainly exert their anesthetic actions via GABA A receptor (GABAA-R). The GABAA-R activity is influenced by phospholipase C-related inactive protein type-1 (PRIP-1), which is related to trafficking and subcellular localization of GABAA-R. PRIP-1 deficiency attenuates the behavioral reactions to propofol but not etomidate. However, the effect of these anesthetics and of PRIP-1 deficiency on brain activity of CNS are still unclear. In this study, we examined the effects of propofol and etomidate on the electroencephalogram (EEG). Methods: The cortical EEG activity was recorded in wild-type (WT) and PRIP-1 knockout (PRIP-1 KO) mice. All recorded EEG data were offline analyzed, and the power spectral density and 95% spectral edge frequency of EEG signals were compared between genotypes before and after injections of anesthetics. Results: PRIP-1 deficiency induced increases in EEG absolute powers, but did not markedly change the relative spectral powers during waking and sleep states in the absence of anesthesia. Propofol administration induced increases in low-frequency relative EEG activity and decreases in SEF95 values in WT but not in PRIP-1 KO mice. Following etomidate injection, low-frequency EEG power was increased in both genotype groups. At high frequency, the relative power in PRIP-1 KO mice was smaller than that in WT mice. Conclusions: The lack of PRIP-1 disrupted the EEG power distribution, but did not affect the depth of anesthesia after etomidate administration. Our analyses suggest that PRIP-1 is differentially involved in anesthetic EEG activity with the regulation of GABAA-R activity.

AB - Purpose: The general anesthetics propofol and etomidate mainly exert their anesthetic actions via GABA A receptor (GABAA-R). The GABAA-R activity is influenced by phospholipase C-related inactive protein type-1 (PRIP-1), which is related to trafficking and subcellular localization of GABAA-R. PRIP-1 deficiency attenuates the behavioral reactions to propofol but not etomidate. However, the effect of these anesthetics and of PRIP-1 deficiency on brain activity of CNS are still unclear. In this study, we examined the effects of propofol and etomidate on the electroencephalogram (EEG). Methods: The cortical EEG activity was recorded in wild-type (WT) and PRIP-1 knockout (PRIP-1 KO) mice. All recorded EEG data were offline analyzed, and the power spectral density and 95% spectral edge frequency of EEG signals were compared between genotypes before and after injections of anesthetics. Results: PRIP-1 deficiency induced increases in EEG absolute powers, but did not markedly change the relative spectral powers during waking and sleep states in the absence of anesthesia. Propofol administration induced increases in low-frequency relative EEG activity and decreases in SEF95 values in WT but not in PRIP-1 KO mice. Following etomidate injection, low-frequency EEG power was increased in both genotype groups. At high frequency, the relative power in PRIP-1 KO mice was smaller than that in WT mice. Conclusions: The lack of PRIP-1 disrupted the EEG power distribution, but did not affect the depth of anesthesia after etomidate administration. Our analyses suggest that PRIP-1 is differentially involved in anesthetic EEG activity with the regulation of GABAA-R activity.

UR - http://www.scopus.com/inward/record.url?scp=85069529511&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85069529511&partnerID=8YFLogxK

U2 - 10.1007/s00540-019-02663-z

DO - 10.1007/s00540-019-02663-z

M3 - Article

VL - 33

SP - 531

EP - 542

JO - Journal of Anesthesia

JF - Journal of Anesthesia

SN - 0913-8668

IS - 4

ER -