PubMed · 9739264
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Y D'Arcy. 1998. Controlling postoperative nausea.. https://pubmed.ncbi.nlm.nih.gov/9739264/
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Mitragynine (1) is a major alkaloidal component in the Thai traditional medicinal herb, Mitragyna speciosa, and has been proven to exhibit analgesic activity mediated by opioid receptors. By utilizing this natural product as a lead compound, synthesis of some derivatives, evaluations of the structure-activity relationship, and surveys of the intrinsic activities and potencies on opioid receptors were performed with guinea pig ileum. The affinities of some compounds for mu-, delta-, and kappa-receptors were determined in a receptor binding assay. The essential structural moieties in the Corynanthe type indole alkaloids for inducing the opioid agonistic activity were also clarified. The oxidative derivatives of mitragynine, i.e., mitragynine pseudoindoxyl (2) and 7-hydroxymitragynine (12), were found as opioid agonists with higher potency than morphine in the experiment with guinea pig ileum. In addition, 2 induced an analgesic activity in the tail flick test in mice.
Intrathecal administration of 5-HT(2) receptor agonists produces an anti-allodynic effect in a rat model of neuropathic pain. Several non-serotonergic neurotransmitters have been implicated these anti-nociceptive effects. In the present study, intrathecal pre-treatment with the muscarinic receptor antagonist atropine (10 and 30 microg) and pirenzepine (10 microg) reversed the anti-allodynic effect of the 5-HT(2) receptor agonist alpha-methyl-5-hydroxytryptamine, unlike various other antagonists. Thus, muscarinic receptors may be involved in the anti-allodynic action of intrathecally injected 5-HT(2) receptor agonist.
We investigated the role of spinal opioid receptors in the antinociceptive effect of kyotorphin (Tyr-Arg, KTP) by using an in vivo mice tail-pinch test and an in vitro opioid receptor binding assays. Intrathecal administration of KTP produced a dose-dependent antinociceptive effect with an ED(50) value of 24 microg/mouse. This antinociception, which was reversed by the KTP antagonist Leu-Arg, was completely blocked by naltrindole but not by naloxonazine, beta-funaltrexamine, or nor-binaltorphimine. The results from the binding study in vitro indicated that KTP bound to spinal KTP receptors but not to any opioid receptors in the mouse spinal cord. These results suggest that KTP-induced antinociception is mediated by binding to KTP receptors followed by an indirect activation of the delta-opioid receptors in the spinal cord.