Propofol-induced anesthesia in mice is mediated by γ-aminobutyric acid-A and excitatory amino acid receptors

Masahiro Irifune, Tohru Takarada, Yoshitaka Shimizu, Chie Endo, Sohtaro Katayama, Toshihiro Dohi, Michio Kawahara

Research output: Contribution to journalArticlepeer-review

75 Citations (Scopus)

Abstract

To elucidate the role of γ-aminobutyric acid (GABA)A receptor complex and excitatory amino acid receptors (N-methyl-D-aspartate [NMDA] and non-NMDA receptors) in propofol-induced anesthesia, we examined behaviorally the effects of GABAergic and glutamatergic drugs on propofol anesthesia in mice. All drugs were administered intraperitoneally. General anesthetic potencies were evaluated using a righting reflex assay. The GABAA receptor agonist muscimol potentiated propofol (140 mg/kg; 50% effective dose for loss of righting reflex) induced anesthesia. Similarly, the benzodiazepine receptor agonist diaze-pain and the NMDA receptor antagonist MK-801 augmented propofol anesthesia, but the non-NMDA receptor antagonist CNQX did not. In contrast, the GABAA receptor antagonist bicuculline antagonized propofol (200 mg/ kg; 95% effective dose for loss of righting reflex) induced anesthesia. However, neither the benzodiazepine receptor antagonist flumazenil, the GABA synthesis inhibitor L-allylglycine, nor the NMDA receptor agonist NMDA reversed propofol anesthesia. Conversely, the non-NMDA receptor agonist kainate enhanced propofol anesthesia. These results suggest that propofol-induced anesthesia is mediated, at least in part, by both GABAA and excitatory amino acid receptors.

Original languageEnglish
Pages (from-to)424-429
Number of pages6
JournalAnesthesia and Analgesia
Volume97
Issue number2
DOIs
Publication statusPublished - Aug 1 2003
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Anesthesiology and Pain Medicine

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