PubMed · 13008030
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E H SEWARD. 1953. Insect nerve blocks?. https://doi.org/10.1111/j.1365-2044.1953.tb12289.x
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The present study was designed to investigate whether endoplasmic inositol 1,4,5-trisphosphate (IP3) receptor-mediated intracellular signaling pathway could be involved in the morphine-induced antinociception in the mouse. An intracerebroventricular (i.c.v.) pretreatment with xestospongin C (10-100 pmol per mouse, i.c.v.), a membrane permeable and selective antagonist for IP3 receptor, produced a dose-dependent reduction in the supraspinal antinociceptive effect produced by i.c.v. administration of morphine (0.3-10 nmol). In addition, the dose-response curve for morphine-induced antinociception was significantly shifted to the right by i.c.v. pretreatment with xestospongin C at 100 pmol. In the present study, we confirmed that the IP3R1 mRNA in opisthonos (opt) heterozygote mice was approximately 50% reduced as compared to that in wild-type mice. Under these conditions, a significant antinociception produced by subcutaneous (s.c.) injection of morphine (5 mg/kg) observed in wild-type mice was markedly reduced in opt heterozygote mice. These findings suggest that IP3 receptor-, especially type 1 IP3 receptor-mediated intracellular signaling pathway may be implicated in the expression of antinociceptive effect induced by morphine in mice.
Nocistatin (NST) and nociception/orphanin FQ (OFQ) are peptides derived from the same precursor that play opposing roles in pain modulation. OFQ antagonizes morphine analgesia and electroacupuncture (EA)-induced antinociceptive effect. The present study investigates whether NST potentiates EA-induced antinociceptive effect and reverses chronic tolerance to EA in mice. Injection of NST (0.5, 5.0 and 50.0 ng) intracerebroventricularly had no effect on basal thermal latency, but produced a dose-dependent potentiation of EA-induced antinociceptive effect in mice with the maximum response at 5.0 ng. NST (5.0 ng) partly reversed chronic tolerance to EA. These results suggest that NST in the brain might play roles in EA-induced antinociceptive effect and the development of chronic tolerance to EA in mice.
We investigated the anti-hyperalgesic effect of FR140423, 3-(difluoromethyl)-1-(4-methoxyphenyl-5-[4-(methylsulfinyl)phenyl]pyrazole, in a rat model of postoperative pain. Oral administration of FR140423 at doses between 1 and 100 mg/kg after surgery dose dependently attenuated the punctate mechanical hyperalgesia caused by an incision of the plantar surface of the hind paw with an ED50 value of 59 mg/kg. The anti-hyperalgesic effect of systematically administered FR140423 was blocked by naloxone, a non-selective opioid receptor antagonist. Furthermore, the delta-opioid receptor antagonist naltrindole (0.2 mg/kg) reversed anti-hyperalgesia induced by FR140423. Naloxonazine and nor-binaltorphimine failed to antagonize the anti-hyperalgesic effect of FR140423. The action of FR140423 differs from the naloxonazine-reversible anti-hyperalgesia induced by morphine. The present findings suggest that delta-opioid systems play a role in the rat anti-hyperalgesia produced by FR140423 for postoperative pain characterized by mechanical hyperalgesia.