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Sevoflurane inhibits presynaptic calcium influx without affecting presynaptic action potentials in hippocampal CA1 region

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Title: Sevoflurane inhibits presynaptic calcium influx without affecting presynaptic action potentials in hippocampal CA1 region
Authors: Hasegawa, Kan Browse this author
Kamiya, Haruyuki Browse this author →KAKEN DB
Morimoto, Yuji Browse this author →KAKEN DB
Issue Date: 1-Oct-2018
Publisher: Biomedical Research Press
Journal Title: Biomedical Research
Volume: 39
Issue: 5
Start Page: 223
End Page: 230
Publisher DOI: 10.2220/biomedres.39.223
PMID: 30333429
Abstract: Although diverse effects of volatile anesthetics have been investigated in various studies, the mechanisms of action of such anesthetics, especially sevoflurane, remain elusive. In contrast to their potent modulation of inhibitory synaptic transmission there is little information about their effects on excitatory transmission in the brain. In this study, we examined the effect of sevoflurane on the excitatory synaptic transmission at CA1 synapses in hippocampal slices of mice. Sevoflurane at 5% was mixed with 95% O-2 and 5% CO2 and bubbled in artificial cerebral spinal fluid (0.69 mM). Extracellular recordings of the field excitatory postsynaptic potential (fEPSP) and presynaptic fiber volley (FV) were made at physiological temperature. In addition, fluorescent measurements of presynaptic Ca2+ transients were performed while simultaneously recording fEPSP. Application of sevoflurane reduced the amplitude of fEPSP (45 +/- 8%, n = 5). This effect was accompanied by concurrent enhancement of the paired-pulse facilitation of fEPSP (127 +/- 5%, n = 12), suggesting a possible presynaptic site of action of sevoflurane. The amplitude of FV was not significantly affected (102 +/- 5%, n = 5). In contrast, fluorescent measurements revealed that presynaptic Ca2+ influx was suppressed by sevoflurane (69 +/- 5%, n = 7), as was simultaneously recorded fEPSP (44 +/- 5%, n = 7). Our results suggest that sevoflurane potently suppresses excitatory synaptic transmission via inhibition of presynaptic Ca2+ influx without affecting presynaptic action potentials.
Type: article
URI: http://hdl.handle.net/2115/72156
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 森本 裕二

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