Spinal Α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic Acid Receptors May Mediate the Analgesic Effects of Emulsified Halogenated Anaesthetics

Hang, Li-Hua; Shao, Donghua; Yang, Yaojing; Ti-jun, Dai; Yin-ming, Zeng

doi:10.1111/j.1440-1681.2007.04690.x

Cited by 4 publications

(3 citation statements)

References 29 publications

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“…Previous studies support the efficacy and safety of the iv administration of emulsified inhalation anesthetics in animals [34,35]. According to drug pharmacokinetics and our preliminary experiments [6,7], we confirmed that ip and sc injection of emulsified inhalation anesthetics can achieve hypnosis and analgesia similar to that produced by inhalation. In the hypnosis test, hypnotic doses of emulsified sevoflurane induced the loss of mouse righting reflex.…”

Section: Discussionsupporting

confidence: 80%

Involvement of 5-hydroxytryptamine type 3 receptors in sevoflurane-induced hypnotic and analgesic effects in mice

Hang

Shao

Wang

et al. 2010

Pharmacological Reports

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Abstract:In the present study, we investigated the role of 5-hydroxytryptamine type 3 (5-HT 3 ) receptors in hypnosis and analgesia induced by emulsified sevoflurane. A mouse model of hypnosis and analgesia was established by an intraperitoneal or subcutaneous injection of emulsified sevoflurane. We intracerebroventricularly (icv) or intrathecally (it) administered YM-31636, a 5-HT 3 receptor agonist, to mice and observed sleep time during hypnosis. In addition, the tail withdrawal latency was measured using the tail withdrawal test, and the writhing time was determined using the acetic acid writhing test. In the hypnosis test, YM-31636 (5, 10 and 15 µg, icv) treatment significantly decreased emulsified sevoflurane-induced mouse sleep time (p < 0.05 or p < 0.01). YM-31636 (2.5, 5 and 10 µg, it) treatment significantly and dose-dependently decreased the tail withdrawal latency (p < 0.05 or p < 0.01) and increased the writhing time (p < 0.01) of mice treated with emulsified sevoflurane. These results suggest that 5-HT 3 receptors may modulate the hypnotic and analgesic effects induced by emulsified sevoflurane.

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Section: Discussionsupporting

confidence: 80%

Involvement of 5-hydroxytryptamine type 3 receptors in sevoflurane-induced hypnotic and analgesic effects in mice

Hang

Shao

Wang

et al. 2010

Pharmacological Reports

Self Cite

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“…There is evidence that activation of NO synthase (NOS), with consequent production of NO, triggered by NMDA receptor activation plays an important role in central and peripheral modulation of nociception 8 . Because isoflurane is certainly able to act as an antagonist at spinal NMDA receptors to produce antinociception, 9,10 it is possible that it may influence NO production. If the NMDA receptors that are blocked by isoflurane are also linked to NO synthesis and release, then it is reasonable to predict that pretreatment with intrathecal injection of the NO precursor l ‐arginine would reduce the antinociceptive effects produced by isoflurane.…”

Section: Introductionmentioning

confidence: 99%

Evidence That Inhibition of Spinal Nitric Oxide Production Contributes to the Antinociceptive Effects of Emulsified Isoflurane on Formalin‐induced Pain in Rats

Zhang

Tan

Zhao³

et al. 2008

Clin Exp Pharma Physio

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The aim of the present study was to investigate the contribution of spinal nitric oxide (NO) to the antinociceptive effects of emulsified isofluane in rats. The formalin test was used to assess nociceptive responses. Immunocytochemistry and histochemistry were performed to determine the effects of emulsified isoflurane on formalin-induced changes in Fos-like immunoreactive (Fos-LI)- and nicotinamide adenine dinucleotide phosphatediaphorase (NADPH-d)-positive neurons, respectively. The results showed that emulsified isofluane, administered intraperitoneally, significantly decreased the formalin-induced paw licking time and that this was attenuated by pretreatment with intrathecal injection of the NO precursor L-arginine. Furthermore, Fos-LI- and NADPH-d-positive neurons were mainly found in the ipsilateral dorsal horn after injection of formalin, some of which were Fos-LI/NADPH-d double-labelled neurons. Administration of emulsified isofluane significantly decreased Fos-LI- and NADPH-d-positive, as well as Fos-LI/NADPH-d double-labelled, neurons. Finally, emulsified isofluane produced a significant reduction of NOS activity and a decrease of NO production in the spinal cord of formalin-treated rats. In conclusion, the results suggest that inhibition of spinal NO production contributes to the antinociceptive effects of emulsified isofluane on formalin-induced pain in rats.

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“…Various in vitro studies have found that the enhancement of inhibitory neurotransmitter function and inhibition of excitatory neurotransmitter function to be plausible mechanisms underlying the action of inhalation anesthetics. Analgesic effects of anesthetics may be related to alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor [4,5,6], benzodiazepine receptor [7], N-methyl-D-Aspartate receptor [8,9,10], glycine receptor [11,12,13,14], nerve nicotinic receptors [15], and alpha 2 receptors [16] on the spinal cord. Morphological and molecular biology research has indicated that the 5-serotonin receptor 1A (5-HT 1A R) is widely distributed in the nervous system.…”

mentioning

confidence: 99%

5-HT<sub>1A</sub> Receptors Mediate Analgesia Induced by Emulsified Sevoflurane in Thermal Nociception but Have Little Effect on Chemical Nociception

Chen

Ti-jun²,

Li³

et al. 2017

Pharmacology

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Objective: The study aimed to investigate the relationship between the analgesic effect of sevoflurane and 5-serotonin receptor 1A (5-HT_1A R) in the spinal cords of mice. Methods: Analgesic mouse models were established by intraperitoneal injection of emulsified sevoflurane, and the influence of p-MPPF (a specific antagonist of 5-HT_1A Rs) intrathecal injection on the changes in tail-flick latency in tail-withdrawal test, pain threshold in hot-plate test (HPPT), and writhing times in acetic acid-induced writhing test were recorded. Results: Intraperitoneal injection of emulsified sevoflurane alone produced an analgesic effect (p < 0.05). p-MPPF (2, 4, and 8 μg) alone had no impact on tail-flick latency, HPPT, and writhing times in mice (p > 0.05). The 3 doses of p-MPPF reduced the tail-flick latency or HPPT. p-MPPF 8 μg can increase the writhing times (p < 0.05) in analgesic mice with sevoflurane, while p-MPPF 2 and 4 μg did not affect the writhing times. Conclusion: 5-HT_1A Rs in the spinal cord may be an important target for the analgesic effect of sevoflurane on the thermal nociception, but it has little relation to the anti-chemical chemical nociceptive effect of sevoflurane.

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Spinal Α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic Acid Receptors May Mediate the Analgesic Effects of Emulsified Halogenated Anaesthetics

Cited by 4 publications

References 29 publications

Involvement of 5-hydroxytryptamine type 3 receptors in sevoflurane-induced hypnotic and analgesic effects in mice

Involvement of 5-hydroxytryptamine type 3 receptors in sevoflurane-induced hypnotic and analgesic effects in mice

Evidence That Inhibition of Spinal Nitric Oxide Production Contributes to the Antinociceptive Effects of Emulsified Isoflurane on Formalin‐induced Pain in Rats

5-HT<sub>1A</sub> Receptors Mediate Analgesia Induced by Emulsified Sevoflurane in Thermal Nociception but Have Little Effect on Chemical Nociception

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