European journal of pain : EJP
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Chemotherapy-induced peripheral neuropathy is a serious side effect in cancer treatment, a major manifestation being neuropathic pain that can be debilitating and can reduce the quality of life of the patient. Oxaliplatin and taxol are common anti-cancer drugs that induce neuropathic pain by an unknown mechanism. We tested the hypothesis that satellite glial cells in dorsal root ganglia (DRGs) are altered in chemotherapy-induced peripheral neuropathy models and contribute to neuropathic pain. ⋯ We propose that increased coupling by gap junctions is part of satellite glial cell activation, and that augmented coupling contributes to the lowering of pain threshold in oxaliplatin- and taxol-treated mice. We further propose that gap junction blockers may have potential in treating chemotherapy-induced neuropathic pain.
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Osteoarthritis (OA) is a highly prevalent, age-related pain condition that poses a significant clinical problem. Here, in the monosodium iodoacetate (MIA) model of OA, we have characterized pain behaviours and associated changes at the first pain synapse in the dorsal horn of the spinal cord. ⋯ Intra-articular MIA is associated with referred mechanical hypersensitivity and increased release of CGRP from primary afferent fibres in the dorsal horn where second-order neuron activation is associated with a microglial response. Antagonism of CGRP receptor activation provides a therapeutic avenue for the treatment of pain in OA.
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Spinal cord stimulation (SCS) is used for the management of chronic intractable neuropathic pain. While used clinically, it is unclear if SCS produces its effects by activation of opioid receptors. The current study aimed to determine if endogenous opioids mediate the analgesia produced by SCS at different frequencies of stimulation in rats with neuropathic pain [spared nerve injury (SNI) model]. ⋯ These results suggest that both 4- and 60-Hz SCS, in part, work through opioid receptor mechanisms, with 4-Hz SCS activating μ-opioid receptors while 60-Hz SCS activated δ-opioid receptors.
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Some recent studies have provided evidence that alteration in central motor control may have causative impact on the emergence and sustenance of chronic pain. We hypothesized that comparison of postural control between patients with high (HP) and low pain (LP) level would display intergroup differences in favour of the LP group lending support for the postulated relationship between altered cortical function and pain. ⋯ Body balance measurements seemed to confirm the hypothesized role of the altered executive function in the CLBP problems, with a further support from pain assessment that indicated central sensitization. Patients with higher self-reported pain level displayed deficit in the postural adaptability to environmental challenge and lower level of postural automaticity.
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Peripheral nerve injury induces up-regulation of the calcium channel alpha-2-delta-1 proteins in the dorsal root ganglia and dorsal spinal cord that correlates with neuropathic pain development. Similar behavioural hypersensitivity was also observed in injury-free transgenic (TG) mice over-expressing the alpha-2-delta-1 proteins in neuronal tissues. To investigate pathways regulating alpha-2-delta-1 protein-mediated behavioural hypersensitivity, we examined whether spinal serotonergic 5-HT3 receptors are involved similarly in the modulation of behavioural hypersensitivity induced by either peripheral nerve injury in a nerve injury model or neuronal alpha-2-delta-1 over-expression in the TG model. ⋯ Our data suggest that spinal 5-HT3 receptors are likely to play a role in alpha-2-delta-1-mediated behavioural hypersensitivities through a descending serotonergic facilitation.