Sevoflurane modulates both GABA(A) and GABA(B) receptors in area CA1 of rat hippocampus

K. Hirota; S. H. Roth

doi:10.1093/bja/78.1.60

Sevoflurane modulates both GABA(A) and GABA(B) receptors in area CA1 of rat hippocampus

K. Hirota^*, S. H. Roth

^*この論文の責任著者

麻酔科学講座

研究成果: ジャーナルへの寄稿 › 学術論文 › 査読

45 被引用数 (Scopus)

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It has been suggested that volatile anaesthetics enhance synaptic inhibition via γ-aminobutyric acid (GABA) in the central nervous system. We have examined the effects of sevoflurane on GABA(A) and GABA(B) receptors in rat hippocampus in vitro. Extracellular recordings were used to record field potentials in rat CA1 pyramidal neurones of transverse hippocampal slices, stimulated electrically via stratum radiatum input. Sevoflurane 0.4-5.0 vol% decreased the amplitudes of population spikes (PS) of CA1 neurones in a concentration-dependent (calculated ED₅₀ = 6.31 vol%) and reversible manner. The GABA(A) antagonist, bicuculline methiodide 5 x 10^-5 mol litre^-1 induced oscillations (multiple spikes) and blocked the inhibitory actions of sevoflurane in the initial component (up to 24.8 ms) of the oscillation. The latter portion of the oscillation (greater than 24.8 ms) was depressed by sevoflurane. The GABA(B) antagonist, phaclofen 5 x 10^-4 mol litre^-1 partially blocked the effects of sevoflurane on the latter portion of the bicuculline-induced oscillation. Sevoflurane 2.0 vol% significantly enhanced paired-pulse (PS2/PS1) facilitation (from 128.4% to 155.5% at an inter-stimulus interval of 37.9 ms); this enhancement was blocked by phaclofen. Stimulus-response relationships revealed that 2.0 vol% sevoflurane increased the intensity of threshold for PS generation to 109.8% of control. Both the GABA(A) agonist, muscimol 2 x 10^-5 mol litre^-1 and the GABA(B) agonist, (±)-baclofen 10^-5 mol litre^-1, potentiated the effects of sevoflurane. Sevoflurane enhanced thresholds by 137.1% and 138.5% of control in the presence of muscimol and (±) baclofen, respectively. The results demonstrate that sevoflurane at clinical concentrations activated both GABA(A)- and GABA(B)-mediated inhibitions in area CA1 of the hippocampus, and that sevoflurane and GABA agonists (muscimol and baclofen) acted on different domains on the GABA(A) and GABA(B) receptors, respectively.

本文言語	英語
ページ（範囲）	60-65
ページ数	6
ジャーナル	British Journal of Anaesthesia
巻	78
号	1
DOI	https://doi.org/10.1093/bja/78.1.60
出版ステータス	出版済み - 1997/01

ASJC Scopus 主題領域

麻酔学および疼痛医療

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10.1093/bja/78.1.60

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title = "Sevoflurane modulates both GABA(A) and GABA(B) receptors in area CA1 of rat hippocampus",

abstract = "It has been suggested that volatile anaesthetics enhance synaptic inhibition via γ-aminobutyric acid (GABA) in the central nervous system. We have examined the effects of sevoflurane on GABA(A) and GABA(B) receptors in rat hippocampus in vitro. Extracellular recordings were used to record field potentials in rat CA1 pyramidal neurones of transverse hippocampal slices, stimulated electrically via stratum radiatum input. Sevoflurane 0.4-5.0 vol% decreased the amplitudes of population spikes (PS) of CA1 neurones in a concentration-dependent (calculated ED50 = 6.31 vol%) and reversible manner. The GABA(A) antagonist, bicuculline methiodide 5 x 10-5 mol litre-1 induced oscillations (multiple spikes) and blocked the inhibitory actions of sevoflurane in the initial component (up to 24.8 ms) of the oscillation. The latter portion of the oscillation (greater than 24.8 ms) was depressed by sevoflurane. The GABA(B) antagonist, phaclofen 5 x 10-4 mol litre-1 partially blocked the effects of sevoflurane on the latter portion of the bicuculline-induced oscillation. Sevoflurane 2.0 vol% significantly enhanced paired-pulse (PS2/PS1) facilitation (from 128.4% to 155.5% at an inter-stimulus interval of 37.9 ms); this enhancement was blocked by phaclofen. Stimulus-response relationships revealed that 2.0 vol% sevoflurane increased the intensity of threshold for PS generation to 109.8% of control. Both the GABA(A) agonist, muscimol 2 x 10-5 mol litre-1 and the GABA(B) agonist, (±)-baclofen 10-5 mol litre-1, potentiated the effects of sevoflurane. Sevoflurane enhanced thresholds by 137.1% and 138.5% of control in the presence of muscimol and (±) baclofen, respectively. The results demonstrate that sevoflurane at clinical concentrations activated both GABA(A)- and GABA(B)-mediated inhibitions in area CA1 of the hippocampus, and that sevoflurane and GABA agonists (muscimol and baclofen) acted on different domains on the GABA(A) and GABA(B) receptors, respectively.",

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author = "K. Hirota and Roth, {S. H.}",

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T1 - Sevoflurane modulates both GABA(A) and GABA(B) receptors in area CA1 of rat hippocampus

AU - Hirota, K.

AU - Roth, S. H.

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N2 - It has been suggested that volatile anaesthetics enhance synaptic inhibition via γ-aminobutyric acid (GABA) in the central nervous system. We have examined the effects of sevoflurane on GABA(A) and GABA(B) receptors in rat hippocampus in vitro. Extracellular recordings were used to record field potentials in rat CA1 pyramidal neurones of transverse hippocampal slices, stimulated electrically via stratum radiatum input. Sevoflurane 0.4-5.0 vol% decreased the amplitudes of population spikes (PS) of CA1 neurones in a concentration-dependent (calculated ED50 = 6.31 vol%) and reversible manner. The GABA(A) antagonist, bicuculline methiodide 5 x 10-5 mol litre-1 induced oscillations (multiple spikes) and blocked the inhibitory actions of sevoflurane in the initial component (up to 24.8 ms) of the oscillation. The latter portion of the oscillation (greater than 24.8 ms) was depressed by sevoflurane. The GABA(B) antagonist, phaclofen 5 x 10-4 mol litre-1 partially blocked the effects of sevoflurane on the latter portion of the bicuculline-induced oscillation. Sevoflurane 2.0 vol% significantly enhanced paired-pulse (PS2/PS1) facilitation (from 128.4% to 155.5% at an inter-stimulus interval of 37.9 ms); this enhancement was blocked by phaclofen. Stimulus-response relationships revealed that 2.0 vol% sevoflurane increased the intensity of threshold for PS generation to 109.8% of control. Both the GABA(A) agonist, muscimol 2 x 10-5 mol litre-1 and the GABA(B) agonist, (±)-baclofen 10-5 mol litre-1, potentiated the effects of sevoflurane. Sevoflurane enhanced thresholds by 137.1% and 138.5% of control in the presence of muscimol and (±) baclofen, respectively. The results demonstrate that sevoflurane at clinical concentrations activated both GABA(A)- and GABA(B)-mediated inhibitions in area CA1 of the hippocampus, and that sevoflurane and GABA agonists (muscimol and baclofen) acted on different domains on the GABA(A) and GABA(B) receptors, respectively.

AB - It has been suggested that volatile anaesthetics enhance synaptic inhibition via γ-aminobutyric acid (GABA) in the central nervous system. We have examined the effects of sevoflurane on GABA(A) and GABA(B) receptors in rat hippocampus in vitro. Extracellular recordings were used to record field potentials in rat CA1 pyramidal neurones of transverse hippocampal slices, stimulated electrically via stratum radiatum input. Sevoflurane 0.4-5.0 vol% decreased the amplitudes of population spikes (PS) of CA1 neurones in a concentration-dependent (calculated ED50 = 6.31 vol%) and reversible manner. The GABA(A) antagonist, bicuculline methiodide 5 x 10-5 mol litre-1 induced oscillations (multiple spikes) and blocked the inhibitory actions of sevoflurane in the initial component (up to 24.8 ms) of the oscillation. The latter portion of the oscillation (greater than 24.8 ms) was depressed by sevoflurane. The GABA(B) antagonist, phaclofen 5 x 10-4 mol litre-1 partially blocked the effects of sevoflurane on the latter portion of the bicuculline-induced oscillation. Sevoflurane 2.0 vol% significantly enhanced paired-pulse (PS2/PS1) facilitation (from 128.4% to 155.5% at an inter-stimulus interval of 37.9 ms); this enhancement was blocked by phaclofen. Stimulus-response relationships revealed that 2.0 vol% sevoflurane increased the intensity of threshold for PS generation to 109.8% of control. Both the GABA(A) agonist, muscimol 2 x 10-5 mol litre-1 and the GABA(B) agonist, (±)-baclofen 10-5 mol litre-1, potentiated the effects of sevoflurane. Sevoflurane enhanced thresholds by 137.1% and 138.5% of control in the presence of muscimol and (±) baclofen, respectively. The results demonstrate that sevoflurane at clinical concentrations activated both GABA(A)- and GABA(B)-mediated inhibitions in area CA1 of the hippocampus, and that sevoflurane and GABA agonists (muscimol and baclofen) acted on different domains on the GABA(A) and GABA(B) receptors, respectively.

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KW - Brain, hippocampus

KW - Rat

KW - Receptors, amino acid

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JO - British Journal of Anaesthesia

JF - British Journal of Anaesthesia

IS - 1

ER -

Sevoflurane modulates both GABA(A) and GABA(B) receptors in area CA1 of rat hippocampus

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