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Amnestic concentrations of sevoflurane inhibit synaptic plasticity of hippocampal CA1 neurons through gamma-aminobutyric acid-mediated mechanisms.
Anesthesiology. 2008 Mar; 108(3):447-56.A

Abstract

BACKGROUND

The cellular mechanisms of anesthetic-induced amnesia are still poorly understood. The current study examined sevoflurane at various concentrations in the CA1 region of rat hippocampal slices for effects on excitatory synaptic transmission and on long-term potentiation (LTP), as a possible mechanism contributing to anesthetic-induced loss of recall.

METHODS

Population spikes and field excitatory postsynaptic potentials were recorded using extracellular electrodes after electrical stimulation of Schaffer-collateral-commissural fiber inputs. Paired pulse facilitation was used as a measure of presynaptic effects of the anesthetic. LTP was induced using tetanic stimulation (100 Hz, 1 s). Sevoflurane at concentrations from amnestic (0.04 mm) to clinical concentrations (0.23-0.41 mm) were added to the perfusion solution.

RESULTS

In the presence of 0.04 mm sevoflurane, the amplitude of population spikes was significantly depressed, and tetanic stimulation induced only posttetanic potentiation and then failure of LTP. These inhibitory effects were antagonized by bicuculline (10 microm), a gamma-aminobutyric acid type A receptor antagonist. Sevoflurane at 0.23-0.41 mm further depressed the amplitude of field excitatory postsynaptic potentials in a dose-dependent manner and completely blocked LTP. Bicuculline only partially antagonized 0.41 mm sevoflurane-induced profound inhibition of LTP. Sevoflurane at 0.23-0.41 mm, but not at 0.04 mm, significantly increased paired pulse facilitation, suggesting that sevoflurane has presynaptic actions to reduce glutamate release from nerve terminals.

CONCLUSIONS

The current study provides evidence that amnestic concentrations of sevoflurane inhibit LTP of hippocampal CA1 neurons through gamma-aminobutyric acid-mediated mechanisms, and these actions seem to account for the effects of amnestic sevoflurane on synaptic plasticity.

Authors+Show Affiliations

Department of Anesthesiology, Gunma University Graduate School of Medicine, Maebashi City, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18292682

Citation

Ishizeki, Junko, et al. "Amnestic Concentrations of Sevoflurane Inhibit Synaptic Plasticity of Hippocampal CA1 Neurons Through Gamma-aminobutyric Acid-mediated Mechanisms." Anesthesiology, vol. 108, no. 3, 2008, pp. 447-56.
Ishizeki J, Nishikawa K, Kubo K, et al. Amnestic concentrations of sevoflurane inhibit synaptic plasticity of hippocampal CA1 neurons through gamma-aminobutyric acid-mediated mechanisms. Anesthesiology. 2008;108(3):447-56.
Ishizeki, J., Nishikawa, K., Kubo, K., Saito, S., & Goto, F. (2008). Amnestic concentrations of sevoflurane inhibit synaptic plasticity of hippocampal CA1 neurons through gamma-aminobutyric acid-mediated mechanisms. Anesthesiology, 108(3), 447-56. https://doi.org/10.1097/ALN.0b013e318164cfba
Ishizeki J, et al. Amnestic Concentrations of Sevoflurane Inhibit Synaptic Plasticity of Hippocampal CA1 Neurons Through Gamma-aminobutyric Acid-mediated Mechanisms. Anesthesiology. 2008;108(3):447-56. PubMed PMID: 18292682.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Amnestic concentrations of sevoflurane inhibit synaptic plasticity of hippocampal CA1 neurons through gamma-aminobutyric acid-mediated mechanisms. AU - Ishizeki,Junko, AU - Nishikawa,Koichi, AU - Kubo,Kazuhiro, AU - Saito,Shigeru, AU - Goto,Fumio, PY - 2008/2/23/pubmed PY - 2008/3/13/medline PY - 2008/2/23/entrez SP - 447 EP - 56 JF - Anesthesiology JO - Anesthesiology VL - 108 IS - 3 N2 - BACKGROUND: The cellular mechanisms of anesthetic-induced amnesia are still poorly understood. The current study examined sevoflurane at various concentrations in the CA1 region of rat hippocampal slices for effects on excitatory synaptic transmission and on long-term potentiation (LTP), as a possible mechanism contributing to anesthetic-induced loss of recall. METHODS: Population spikes and field excitatory postsynaptic potentials were recorded using extracellular electrodes after electrical stimulation of Schaffer-collateral-commissural fiber inputs. Paired pulse facilitation was used as a measure of presynaptic effects of the anesthetic. LTP was induced using tetanic stimulation (100 Hz, 1 s). Sevoflurane at concentrations from amnestic (0.04 mm) to clinical concentrations (0.23-0.41 mm) were added to the perfusion solution. RESULTS: In the presence of 0.04 mm sevoflurane, the amplitude of population spikes was significantly depressed, and tetanic stimulation induced only posttetanic potentiation and then failure of LTP. These inhibitory effects were antagonized by bicuculline (10 microm), a gamma-aminobutyric acid type A receptor antagonist. Sevoflurane at 0.23-0.41 mm further depressed the amplitude of field excitatory postsynaptic potentials in a dose-dependent manner and completely blocked LTP. Bicuculline only partially antagonized 0.41 mm sevoflurane-induced profound inhibition of LTP. Sevoflurane at 0.23-0.41 mm, but not at 0.04 mm, significantly increased paired pulse facilitation, suggesting that sevoflurane has presynaptic actions to reduce glutamate release from nerve terminals. CONCLUSIONS: The current study provides evidence that amnestic concentrations of sevoflurane inhibit LTP of hippocampal CA1 neurons through gamma-aminobutyric acid-mediated mechanisms, and these actions seem to account for the effects of amnestic sevoflurane on synaptic plasticity. SN - 1528-1175 UR - https://www.unboundmedicine.com/medline/citation/18292682/Amnestic_concentrations_of_sevoflurane_inhibit_synaptic_plasticity_of_hippocampal_CA1_neurons_through_gamma_aminobutyric_acid_mediated_mechanisms_ L2 - https://pubs.asahq.org/anesthesiology/article-lookup/doi/10.1097/ALN.0b013e318164cfba DB - PRIME DP - Unbound Medicine ER -