Pain
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Transient receptor potential ion channel melastatin subtype 8 (TRPM8) is activated by cold temperatures and cooling agents, such as menthol and icilin. Compounds containing peppermint are reported to reduce symptoms of bowel hypersensitivity; however, the underlying mechanisms of action are unclear. Here we determined the role of TRPM8 in colonic sensory pathways. ⋯ Icilin also prevented mechanosensory desensitization and sensitization induced by capsaicin and the TRPA1 agonist AITC (40 μmol/L), respectively. TRPM8 is present on a select population of colonic high threshold sensory neurons, which may also co-express TRPV1. TRPM8 couples to TRPV1 and TRPA1 to inhibit their downstream chemosensory and mechanosensory actions.
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Epinephrine (EPI) contributes to hyperalgesia in inflammatory and stress conditions. EPI signals via adrenoceptors, which are regulated by G protein-coupled receptor kinase 2 (GRK2). We previously reported that GRK2 is decreased in nociceptors during chronic inflammation. ⋯ In terms of EPI signalling pathways, the protein kinase A (PKA) inhibitor H-89 inhibited EPI-induced mechanical hyperalgesia in wild-type mice, whereas H-89 had no effect in mice with low GRK2 in sensory neurons (SNS-GRK2(+/-) mice). Conversely, intraplantar injection of the protein kinase Cε PKCε inhibitor TAT-PKC(εv1-2) inhibited hyperalgesia in sensory neuron specific (SNS)-GRK2(+/-) mice and not in wild-type mice. These results indicate that low GRK2 in primary sensory neurons switches EPI-induced signalling from a protein kinase A-dependent toward a PKCε-dependent pathway that ultimately mediates prolonged EPI-induced hyperalgesia.
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Sick leave due to low back pain (LBP-SL) is costly and compromises workforce productivity. The fear-avoidance model asserts that maladaptive pain-related cognitions lead to avoidance and disuse, which can perpetuate ongoing pain. Staying home from work is an avoidant behavior, and hence pain-related psychological features may help explain LBP-SL. ⋯ Administrators and managers were less likely to report LBP-SL (OR=0.44, 95% CI 0.27-0.71), and age had a protective effect in individuals in a married or de facto relationship (OR=0.97, 95% CI 0.95-0.98). In summary, fear of movement, passive coping, frequent manual handling, and severe or radiating pain increase the likelihood of LBP-SL. Gender-specific responses to pain radiation and fear of movement are evident.
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The shared-representation model of empathy suggests that vicarious pain processes rely partly on the activation of brain systems underlying self-pain in the observer. Here, we tested the hypothesis that self-pain may be facilitated by the vicarious priming of neural systems underlying pain perception. Pictures illustrating painful agents applied to the hand or the foot (sensory information), or painful facial expressions (emotional information) were shown to 43 participants to test the effects of vicarious pain on the nociceptive flexion reflex (NFR) of the lower limb and pain intensity and unpleasantness produced by transcutaneous electrical stimulation applied over the sural nerve. ⋯ In contrast, the change in perceived shock-pain intensity was negatively correlated with empathic traits. This dissociation implies that low-level vicarious priming processes underlying pain facilitation may be downregulated at higher pain-processing stages in individuals reporting higher levels of empathy. We speculate that this process contributes to reducing self-other assimilation and is necessary to adopt higher-order empathic responses and altruistic behaviors.