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Cited by 104Neuroscience and Neuropharmacology ResearchAnesthesia and Sedative AgentsAnesthesia and Neurotoxicity Research

The DOI matches its Crossref record, with a small difference in title or year; 53 of the 53 references it cites were found in a registry or an index.

Effects of Halothane on Glutamate Receptor-mediated Excitatory Postsynaptic Currents: A Patch-Clamp Study in Adult Mouse Hippocampal Slices

Perouansky, Misha, Baranov, Dimitri, Salman, Michael, Yaari, Yoel·1995·Anesthesiology
DOI 10.1097/00000542-199507000-00014
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Abstract

Background: The effects of halothane on excitatory synaptic transmission in the central nervous system of mammals have been studied in vivo and in vitro in several investigations with partially contradicting results. Direct measurements of the effects of halothane on isolated glutamate receptor-mediated (glutamatergic) excitatory postsynaptic currents (EPSCs), however, have not been reported to date. Methods: The effects of halothane on glutamatergic EPSCs were studied in vitro by using tight-seal, whole-cell recordings from CA1 pyramidal cells in thin slices from the adult mouse hippocampus. The EPSCs were pharmacologically isolated into their non-N-methyl-D-aspartate (non-NMDA) and NMDA receptor-mediated components by using selective antagonists. The effects of halothane on EPSC amplitude and kinetics were analyzed at various membrane potentials and were compared with its effects on currents evoked by exogenously applied glutamatergic agonists. Results: Halothane (0.2-5.1%; 0.37-2.78 mM) reversibly blocked non-NMDA and NMDA EPSCs. This effect was voltage independent; concentrations producing 50% inhibition were 0.87% (0.66 mM) and 0.69% (0.57 mM), respectively. Currents induced by bath-applied glutamatergic agonists were not affected even by the high concentrations of halothane. Conclusions: Halothane depresses glutamatergic EPSCs irrespective of receptor subtype, most likely by inhibition of glutamate release.

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Crossref · 10.1097/00000542-199507000-00014

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53 of 53 references verified0 citation errors · 0 not checkable

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  • Anesthetics modulate presynaptic neurotransmitter release as an intrinsic component of their actions.

    “A number of studies point to an important role for anesthetics in modulating presynaptic neurotransmitter release as an intrinsic component of their actions [78–80].”

    From The Biology of General Anesthesia from Paramecium to Primate (2019) · cites this paper as [79]

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Metadata

Authors
Perouansky, M., Baranov, D., Salman, M., & Yaari, Y.
Affiliations
Hebrew University of Jerusalem (IL)
ORCID
Venue
Anesthesiology
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
1995-07-01
Volume
83
Issue
1
Pages
109-119.
ISSN
0003-3022 (ISSN-L)
DOI
10.1097/00000542-199507000-00014
OpenAlex
W1996815194
Cited by
104
References
53
Citations by year
2026: 1 · 2025: 2 · 2024: 1 · 2023: 1 · 2021: 2 · 2020: 2 · 2019: 1 · 2018: 1 · 2016: 2 · 2015: 1 · 2014: 4 · 2012: 5
FWCI
3.03
Type
journal article
Language
en
Open access
closed
Locations
  • Anesthesiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Health Sciences › Medicine › Anesthesiology and Pain Medicine › Anesthesia and Sedative Agents
  • Life Sciences › Neuroscience › Developmental Neuroscience › Anesthesia and Neurotoxicity Research
Keywords
halothane, glutamate receptors, excitatory postsynaptic currents, NMDA receptor, non-NMDA receptors, glutamatergic neurotransmission, CA1 pyramidal neurons, glutamate release inhibition, volatile anesthetics
MeSH terms
Animals, Dose-Response Relationship, Drug, Halothane, Hippocampus, Synapses, Receptors, Glutamate, Patch-Clamp Techniques, Mice, In Vitro Techniques

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