Articles: hyperalgesia.
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Up-regulation of P2X4 receptors in spinal cord microglia is crucial for tactile allodynia, an untreatable pathological pain reaction occurring after peripheral nerve injury. How nerve injury in the periphery leads to this microglia reaction in the dorsal horn of the spinal cord is not yet understood. It is shown here that CCL21 was rapidly expressed in injured small-sized primary sensory neurons and transported to their central terminals in the dorsal horn. ⋯ A single intrathecal injection of CCL21 to nerve-injured CCL21-deficient mice induced long-lasting allodynia that was undistinguishable from the wild-type response. This effect of CCL21 injection was strictly dependent on P2X4 receptor function. Since neuronal CCL21 is the earliest yet identified factor in the cascade leading to tactile allodynia, these findings may lead to a preventive therapy in neuropathic pain.
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Anesthesia and analgesia · May 2011
Central and local administration of Gingko biloba extract EGb 761® inhibits thermal hyperalgesia and inflammation in the rat carrageenan model.
Oral administration of the standardized Ginkgo biloba extract EGb 761® has been shown to inhibit thermal hyperalgesia in rodent models of inflammatory and postsurgical pain, but the mechanism underlying these effects is not known. We sought to determine the site of action of EGb 761 by investigating the antihyperalgesic and antiinflammatory properties of EGb 761 after local and central drug administration in the rat carrageenan model of inflammation. ⋯ These studies show that EGb 761 acts both at the site of inflammation and centrally at the spinal cord level to inhibit inflammation and thermal hyperalgesia, and may be useful in the treatment of inflammatory pain.
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Gabapentin is an anticonvulsant and adjuvant analgesic. It is effective in several pain studies. Neuropathic pain is the most difficult type of pain to treat. In this study, we examined if intrathecal gabapentin could prevent nerve injury-induced pain. ⋯ We showed a preventative effect of intrathecal gabapentin on the development of nerve injury-induced mechanical allodynia and thermal hyperalgesia. Our data suggest that continuous intrathecal gabapentin may be considered as an alternative for the prevention of nerve injury-induced pain.
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The pathogenesis of widespread pain and increased tenderness in Fibromyalgia (FM) are still unknown. Recently, the role of central nervous system hyperexcitability is emphasized in pathogenesis of FM. The central sensitization was demonstrated with decrease in nociceptive flexion reflex (NFR) threshold in patients with FM. The NFR and cutaneous silent period (CuSP) are excitatory and inhibitory parts of the same spinal protective reflex, respectively. The aim of this study was to evaluate the changes in CuSP in FM. ⋯ The latency elongation of the CuSP shows that there is some delay in the development of the inhibitory part of the spinal protective reflex in patients with FM. The observed changes in CuSP of the patients with FM may suggest some abnormalities in the circuits of sensorimotor integration at spinal and supraspinal levels. The results regarding the changes observed in the CuSP in patients with FM should be confirmed by further studies.
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Pharmacol. Biochem. Behav. · May 2011
Formalin-induced long-term secondary allodynia and hyperalgesia are maintained by descending facilitation.
This work analyzes the role of cholecystokinin (CCK) receptors, dynorphin A₁₋₁₇ and descending facilitation originated in the rostral ventromedial medulla (RVM) on secondary allodynia and hyperalgesia in formalin-injected rats. Formalin injection (50 μL, 1%, s.c.) produced acute nociception (lasting 1 h) and long-term secondary allodynia and hyperalgesia in ipsilateral and contralateral hind paws (lasting 1-12 days). Once established, intra-RVM administration of lidocaine at day 6, but not at 2, reversed secondary allodynia and hyperalgesia in rats. ⋯ Moreover, intrathecal administration of dynorphin antiserum reversed, but was unable to prevent, secondary allodynia and hyperalgesia in both hind paws. These results suggest that formalin-induced secondary allodynia and hyperalgesia are maintained by activation of descending facilitatory mechanisms which are dependent on CCK₂ receptors located in the RVM and spinal cord. In addition, data suggest that spinal dynorphin A₁₋₁₇ and CCK play an important role in formalin-induced secondary allodynia and hyperalgesia.