Xenon Reduces N -Methyl-d-aspartate and α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid Receptor–mediated Synaptic Transmission in the Amygdala
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BACKGROUND: The neuronal and molecular targets of the inhalational general anesthetic xenon are a matter of debate. The current knowledge is largely based on studies using neurons in culture or heterologous expression systems. In the current study, the authors evaluated for the first time the effect of xenon on synaptic transmission in the basolateral amygdala in an in vitro brain slice preparation of the mouse. METHODS: A patch clamp technique was used to evaluate the effects of xenon on N-methyl-d-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor-mediated excitatory postsynaptic currents (EPSCs), as well as on gamma-aminobutyric acid type A receptor-mediated inhibitory postsynaptic currents. The currents were either evoked upon electrical stimulation (NMDA-eEPSCs, AMPA-eEPSCs) or upon focal, laser-guided photolysis of caged l-glutamate (p-NMDA-Cs, p-AMPA-Cs). In addition, the authors investigated the effects of xenon on miniature EPSCs. RESULTS: Xenon reversibly reduced basal synaptic transmission but had no effect on gamma-aminobutyric acid type A receptor-mediated inhibitory synaptic transmission. Xenon concentration-dependently diminished NMDA-eEPSCs and p-NMDA-Cs to the same amount. Likewise, xenon-induced reduction of AMPA-eEPSCs and p-AMPA-Cs did not differ. Xenon did not affect the frequency of miniature EPSCs but reduced their amplitude. CONCLUSIONS: In the current study, xenon considerably depressed NMDA and AMPA receptor-mediated synaptic transmission in the basolateral amygdala without affecting inhibitory synaptic transmission. The results provide evidence that the effects of xenon on NMDA- and AMPA-EPSCs are primarily mediated via postsynaptic mechanisms.
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Xenon reduces NMDA-induced synaptic currents and neuronal plasticity in brain areas involved in fear learning and memory, including the amygdala and hippocampus.
“This idea is supported by preclinical findings showing that xenon reduces NMDAinduced synaptic currents and neuronal plasticity in brain areas involved in fear learning and memory processes including the amygdala and hippocampus (Haseneder et al., 2008;Kratzer et al., 2012).”
From Novel pharmacological targets in drug development for the treatment of anxiety and anxiety-related disorders (2019) · cites this paper as Haseneder et al., 2008
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Self-citation
- Authors
- Haseneder, R., Kratzer, S., Kochs, E., Eckle, V.-S., Zieglgänsberger, W., & Rammes, G.
- Affiliations
- Resident in Anesthesia.
- Medical Student.
- Professor of Anesthesiology, Director and Chair.
- Max Planck Institute of Psychiatry (DE)
- TUM Klinikum (DE)
- Venue
- Anesthesiology
- Published
- 2008-12-01
- Volume
- 109
- Issue
- 6
- Pages
- 998-1006
- ISSN
- 0003-3022 (ISSN-L)
- OpenAlex
- W2089994977
- Cited by
- 47
- References
- 40
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 3 · 2023: 4 · 2022: 3 · 2020: 1 · 2019: 7 · 2017: 3 · 2016: 1 · 2015: 3 · 2014: 4 · 2012: 5
- FWCI
- 1.44
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Anesthesiology (publishedVersion)
- PubMed (publishedVersion)
- mediaTUM (Technical University of Munich) (submittedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- 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
- xenon, inhalational anesthetics, NMDA receptor, AMPA receptors, synaptic transmission, basolateral amygdala, excitatory postsynaptic currents, inhibitory postsynaptic currents, GABAA receptor, miniature EPSCs, postsynaptic mechanisms
- MeSH terms
- Amygdala, Animals, Male, Mice, Inbred C57BL, Synaptic Transmission, Xenon, Receptors, N-Methyl-D-Aspartate, Receptors, AMPA, Excitatory Postsynaptic Potentials, Mice
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