Volatile anesthetics and glutamate activation of N-methyl-D-aspartate receptors

Martin, D.C.; Plagenhoef, Marc; Abraham, James; Dennison, Robert L.; Aronstam, Robert S.

doi:10.1016/0006-2952(94)00519-r

Cited by 86 publications

(47 citation statements)

References 20 publications

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“…Later, studies in hippocampal slices and neurons showed that volatile anesthetics depress activation of neuronal responses by NMDA (Yang and Zorumski, 1991;Perouansky et al, 1995). Moreover, various volatile anesthetics inhibit glutamate-stimulated activation of NMDA receptors, measured by the binding of MK-801, a use-dependent NMDA receptor blocker, to rat cerebral cortex (Martin et al, 1995). The role of NMDA receptors in spinal cord in the immobilizing action of anesthetics is also supported by in vivo studies (Stabernack et al, 2003).…”

mentioning

confidence: 96%

Effects of Anesthetics on Mutant N-Methyl-d-Aspartate Receptors Expressed in Xenopus Oocytes

Ogata

Shiraishi

Namba

et al. 2006

J Pharmacol Exp Ther

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Alcohols, inhaled anesthetics, and some injectable anesthetics inhibit the function of N-methyl-D-aspartate (NMDA) receptors, but the mechanisms responsible for this inhibition are not fully understood. Recently, it was shown that ethanol inhibition of NMDA receptors was reduced by mutation of residues in the transmembrane (TM) segment 3 of the NR1 subunit (F639A) or in TM4 of the NR2A subunit (A825W), suggesting putative ethanol binding sites. We hypothesized that the actions of other anesthetics might also require these amino acids and evaluated the effects of anesthetics on the NMDA receptors expressed in Xenopus oocytes with two-electrode voltage-clamp recording.

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mentioning

confidence: 96%

Effects of Anesthetics on Mutant N-Methyl-d-Aspartate Receptors Expressed in Xenopus Oocytes

Ogata

Shiraishi

Namba

et al. 2006

J Pharmacol Exp Ther

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“…9 Moreover, several in vitro electrophysiological and pharmacological studies have demonstrated sevoflurane's anti-NMDA properties. 21,23 The findings from our study suggest that sevoflurane, when administered at concentrations even below the MAC value, might play an anti-hyperalgesic role via an anti-NMDA action.…”

Section: Discussionmentioning

confidence: 74%

“…8,[18][19][20] Halogenated anesthetics have in vitro anti-NMDA properties. [21][22][23][24] Other studies have shown that halogenated anesthetics induce hyperalgesia when administered at very low concentrations 25,26 and even decrease morphine analgesic effects. 25,27 However, in the context of current clinical practice, it is unresolved as to whether or not inhaled anesthetics elicit residual effects on postoperative hyperalgesia.…”

Section: Résumémentioning

confidence: 99%

Effects of sevoflurane on carrageenan- and fentanyl-induced pain hypersensitivity in Sprague-Dawley rats

Richebé

Rivalan

Rivat

et al. 2008

Can J Anesth/J Can Anesth

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Purpose Opioids are widely used for anesthesia but paradoxically induce postoperative pain hypersensitivity via N-methyl-D-aspartate (NMDA) receptor modulation. Sevoflurane effects on opioid-induced hyperalgesia have not been yet evaluated in vivo. Nevertheless, some experimental in vitro studies reported anti-NMDA receptor properties for sevoflurane. The aim of this study was to evaluate sevoflurane effects on fentanyl-induced hyperalgesia in opioid-naive rats and in rats with inflammatory pain. Methods Sevoflurane effects on hyperalgesia were evaluated in Sprague-Dawley rats: opioid-naive rats, rats treated with fentanyl (4 9 60 lg kg -1 ) and rats with inflammatory pain (carrageenan) treated with fentanyl (4 9 60 lg kg -1 ). On day zero, subcutaneous fentanyl injections were administered and inflammatory pain was induced with one carrageenan injection in one hind paw. Rats were exposed to low concentrations of sevoflurane (1.0 or 1.5%) on day zero prior to fentanyl injections and inflammatory pain induction, and for the duration of the fentanyl analgesic effect. The nociceptive threshold (Randall-Selitto test) was evaluated daily for 7 days. On day seven, naloxone was injected and the nociceptive threshold was assessed 5 min later. Results In rats without inflammatory pain but treated with fentanyl on day zero, sevoflurane 1.0% reversed the early (day zero) and long-lasting (day zero to day three) hyperalgesia classically described after high-doses of fentanyl (P \ 0.05). This sevoflurane concentration antagonized the hyperalgesia induced by naloxone on day seven (P = 0.33). In a second experiment in rats with inflammatory pain, exposure to low concentrations of sevoflurane (1.0 and 1.5%) did not reduce fentanyl-induced hyperalgesia (P [ 0.05), but nevertheless antagonized the naloxone induced hyperalgesia on day seven (P = 0.061). Conclusion Relatively low sevoflurane concentrations (1.0%) reverse fentanyl-induced hyperalgesia in rats without inflammatory pain. Nevertheless, the lack of effect of sevoflurane concentrations of 1.0% and 1.5% to oppose hyperalgesia following high-dose fentanyl and inflammatory pain suggests that sevoflurane anti-hyperalgesic properties are weak. RésuméObjectif Les opioı¨des sont largement utilise´s en anesthe´sie mais induisent paradoxalement une hypersensibiliteṕ ostope´ratoire a`la douleur via une modulation des re´cepteurs N-me´thyl-D-aspartate (NMDA). Les effets du

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“…Ketamine is considered an anesthetic (especially an inhalation anesthetic) that works by inhibiting the release of presynaptic glutamate, enhancing the re-uptake of glutamate and blocking the postsynaptic excitatory amino acid receptors (Boveris and Puntarulo, 1998). Several in vitro and in vivo studies demonstrated that volatile compounds depress the central nervous system through the inhibition of glutamate mediated transmission, both via post-synaptic depressant action and pre-synaptic inhibition (Martin et al 1995;Dildly-Mayfield et al, 1996;Miyazaki et al, 1997). The level of circulating glutamate is an important factor influencing the synaptic efficacy.…”

Section: Discussionmentioning

confidence: 99%

Influence of ketamine on amino acid neurotransmitters secretion by nerve cells in vitro

Shi

Chen

Guo

et al. 2016

Bangladesh J Pharmacol

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In order to study the influence of amino acid neurotransmitters secreted by the nerve cells after ketamine treatment, the nerve cells were cultured in vitro to exclude the interference of other factors in vivo and treated with three different doses of ketamine (1, 3 and 5 µg/mL). Then, the concentration of neuronal amino acid neurotransmitters was examined at 0, 15, 30, 45, 60, 90, 120 min after treatment. The trends of each amino acid concentration after ketamine treatment were nearly the same among the different treatment doses. After 15 min of adapting time, ketamine decreased the excitatory amino acid glutamic acid and aspartic acid concentration, and increased the concentration of the inhibitory amino acid glycine. Their concentrations showed a tendency to return approximately to the original level after 120 min.

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Volatile anesthetics and glutamate activation of N-methyl-D-aspartate receptors

Cited by 86 publications

References 20 publications

Effects of Anesthetics on Mutant N-Methyl-d-Aspartate Receptors Expressed in Xenopus Oocytes

Effects of Anesthetics on Mutant N-Methyl-d-Aspartate Receptors Expressed in Xenopus Oocytes

Effects of sevoflurane on carrageenan- and fentanyl-induced pain hypersensitivity in Sprague-Dawley rats

Influence of ketamine on amino acid neurotransmitters secretion by nerve cells in vitro

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