Brief communicationSpinal and supraspinal effects of pertussis toxin on opioid analgesia
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Cited by (29)
Ultra-low dose naloxone restores the antinocicepitve effect of morphine in PTX-treated rats: Association of IL-10 upregulation in the spinal cord
2012, Life SciencesCitation Excerpt :This model has been used as an animal model to study the pathophysiology of neuropathic pain (Womer and Shannon, 2000). Similar phenomenon had been demonstrated in the intrathecal PTX treated animals with reduction of the antinociceptive potency of opioid agonists (Shah et al., 1994). By using the PTX model, Womer et al. (1997) also found that morphine is less effective in treating central and neuropathic pains than treating acute pain (Womer et al., 1997).
Ultra-low-dose naloxone enhances the antinociceptive effect of morphine in PTX-treated rats: Regulation on global histone methylation
2012, Acta Anaesthesiologica TaiwanicaCitation Excerpt :The PTX model had been used to study the pathophysiology of neuropathic pain.12 Certain studies had demonstrated that intrathecal PTX injection could reduce the antinociceptive potency of etorphine, fentanyl,13 and selective μ-agonist PL017.14 Womer et al found that PTX could disrupt the antinociceptive signal transduction of morphine, and therefore reduced morphine's effect in treating central and neuropathic pains than treating acute pain.15
The analgesic efficacy of fentanyl: Relationship to tolerance and μ-opioid receptor regulation
2008, Pharmacology Biochemistry and BehaviorAmitriptyline pretreatment preserves the antinociceptive effect of morphine in pertussis toxin-treated rats by lowering CSF excitatory amino acid concentrations and reversing the downregulation of glutamate transporters
2008, Brain ResearchCitation Excerpt :Intrathecal (i.t.) administration of pertussis toxin (PTX) caused hyperalgesia and allodynia that appears similar to the symptoms reported by patients suffering from neuropathic pain (McCormack et al., 1998). Activation of PTX-sensitive G proteins represents an essential step in the transduction mechanism underlying central antinociception (Galeotti et al., 1996) and PTX can be used as a probe to help uncover the cellular mechanisms of opioid actions (Shah et al., 1994). Following a further characterization of the PTX model, Womer et al. (1997) concluded that the i.t. PTX injection-induced persistent thermal hyperalgesia and allodynia are similar to other neuropathic pain models involving nerve ligation or section (Bennett and Xie, 1988; Kim and Chung, 1992; Wiesenfeld-Hallin, 1984), and they suggested that PTX-induced hyperalgesia and allodynia are not caused by a peripheral mechanism, but via a direct central mechanism (McCormack et al., 1998; Womer et al., 1997).