Pain
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Epibatidine has shown antinociceptive effects in various pain models, being 200-fold more potent than morphine. Previous results from our laboratory demonstrated that HO-1 overexpression has an antinociceptive effect in the formalin test. Furthermore, epibatidine was able to induce haeme oxygenase-1 (HO-1). ⋯ Furthermore, the antinociceptive effect of epibatidine was related to the activation of alpha7 and/or alpha9 nAChRs since methyllycaconitine (MLA) and mecamylamine but not dihydro-beta-erythroidine (DHbetaE) reverted this effect. Finally, we showed by flow cytometry and by immunofluorescence that white blood cells of the animals injected with epibatidine expressed more HO-1 than control animals, and this expression was also reverted by MLA pre-treatment. These findings demonstrate that HO-1 induction by epibatidine has antinociceptive and anti-inflammatory effects by the activation of MLA-sensitive nAChRs.
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Investigated was the relationship between pain catastrophizing and pain intensity in adolescents suffering from chronic pain (n = 38) and the extent to which they expressed communicative pain and pain-related protective behaviours. Adolescents were observed on video performing a 2-Min Walk Test (2MWT). Behaviours were coded on videotape. ⋯ Pain-related protective behaviours did not vary with the adolescents' level of pain catastrophizing, but varied with pain intensity. The findings corroborate the functional distinctiveness of different types of pain behaviours. The results are discussed in terms of the processes linking (1) catastrophizing to communicative pain behaviours and (2) pain to pain-related protective behaviours.
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Sex differences in pain perception have been clearly documented in the literature during the last decades and it has been shown that women perceived more pain than men. Sex hormones (SHs) are thought to be one of the main mechanisms which explain sex differences in pain. Pain is a dynamic phenomenon involving both excitatory and inhibitory mechanisms. ⋯ However, we found significantly more pain inhibition (DNIC effectiveness) during the ovulatory phase compared to the menstrual and luteal phases (p=0.05). The main finding of this study is the observation that only inhibitory mechanisms (DNIC analgesia) and not excitatory pain mechanisms vary throughout the MC, where women have greater DNIC in the ovulatory phase. The higher occurrence of pain and lower pain threshold previously reported during the MC could be related to a reduction in endogenous pain control mechanisms.
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Do contrasting neuropathic pain diagnoses share common pathophysiological mechanisms? Selective breeding was used to derive rat lines with a common genetic background but a striking difference in the degree of spontaneous pain behavior expressed in the neuroma model of neuropathic pain (HA rats (high autotomy) and LA rats (low autotomy)). The contrasting pain phenotype in these lines is attributable to allelic differences at a small number of genetic loci. Here we show that HA and LA rats also differ in their nocifensive response to applied stimuli in the Chung (spinal nerve ligation, SNL) model of neuropathic pain. ⋯ F1 crosses of HA and LA rats and inbred Lewis rats showed low levels of autotomy but variable levels of hypersensibility to applied stimuli. Results indicate that alleles which predispose to spontaneous neuropathic pain also predispose to stimulus-evoked pain (allodynia and hyperalgesia). This, in turn, suggests that despite contrasting etiology and behavioral endpoints, pain phenotype in the neuroma and the SNL models shares common pathophysiological mechanisms.
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Oxaliplatin is a platinum-based chemotherapy drug characterized by the development of a painful peripheral neuropathy which is reproduced in rodent animal models with features observed in humans. Our focus was to explore the alterations of intracellular second messengers at supraspinal level in oxaliplatin-induced mechanical hyperalgesia. In our experiments, chronic administration of oxaliplatin to rats induced mechanical hyperalgesia which lasted for many days. ⋯ Distinct PKC-activated MAPK pathways, including p38MAPK, ERK1/2 and JNK, were investigated in chronic oxaliplatin rat. A dramatic phosphorylation increase, Calphostin C sensitive, could be observed in thalamus and PAG for p38MAPK. These data show that, in oxaliplatin-induced neuropathy, enhanced mechanical nociception is strictly correlated with increased phosphorylation of specific intracellular mediators in PAG and thalamus brain regions pointing to a role of these supraspinal centers in oxaliplatin-induced neuropathic pain mechanism.