Articles: hyperalgesia.
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The heat/capsaicin sensitization and intradermal capsaicin injection models are safe and noninvasive paradigms to generate stable, long-lasting, and reproducible injury capable of producing an area of both primary and secondary hyperalgesia. Risk of skin injury is substantially reduced since lower levels of thermal and chemical irritation produce long-lasting cutaneous hyperalgesia. ⋯ Unlike the heat/capsaicin sensitization model, intradermal capsaicin results in a brief painful stimulus followed by a long lasting area of secondary hyperalgesia. The intradermal injection of capsaicin results in a transient, intense stinging sensation at the site of injection (e.g. heat allodynia) followed by a persistent area of secondary tactile allodynia.
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In this study, we examined the relationship between astrocyte activation in the cuneate nucleus (CN) and behavioral hypersensitivity after chronic constriction injury (CCI) of the median nerve. In addition, we also examined the effects of pre-emptive treatment with a number of drugs on astrocyte activation and hypersensitivity development in this model. Using immunohistochemistry and immunoblotting, little glial fibrillary acidic protein (GFAP; an astrocyte marker) immunoreactivity was detected in the CN of the normal rats. ⋯ Animals received MK-801 (glutamate N-methyl-d-aspartate (NMDA) receptor antagonist), clonidine (alpha(2)-adrenoreceptor agonist), tetrodotoxin (TTX, sodium channel blocker) or lidocaine (local anesthetic) 30 min prior to median nerve CCI. Pre-treatment with MK-801, TTX, and 2% lidocaine, but not clonidine, attenuated GFAP immunoreactivity and behavioral hypersensitivity following median nerve injury. In conclusion, suppressing reactions to injury, such as the generation of ectopic discharges and activation of NMDA receptors, can decrease astrocyte activation in the CN and attenuate neuropathic pain sensations.
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The UV-B pain model utilizes ultraviolet light to induce a small area of inflammation allowing assessment of mechanical and thermal thresholds. Pharmacologic testing has mainly focused on reduction of primary hyperalgesia, although the effect of analgesics on secondary hyperalgesia has also been investigated. The model requires an instrument to precisely generate controlled UV-B tissue hyperalgesia. ⋯ Tissue is then assessed for inflammation using color Doppler imaging or flare measurements. Heat pain thresholds and pain tolerance are often evaluated using a commercially available thermal sensory testing device. Analgesics can be administered to determine the influence on these clinical endpoints.
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Although cold hypersensitivity is a well-documented phenomenon in animals and humans with inflammatory and neuropathic pain, little is known about the presence of cold hyperalgesia after surgery. Therefore, we studied primary cold hyperalgesia after a surgical incision in mice. ⋯ The present data give strong evidence that a surgical incision does not cause cold hyperalgesia. Furthermore, a lack of cold hyperalgesia in unrestrained male and female mice after incision was not due to increased skin temperature after incision. Finally, we demonstrated that in contrast to a surgical incision, inflammation and nerve injury generate intense cold hyperalgesia and an increase in skin temperature, suggesting that different mechanisms are involved in surgical and inflammatory or neuropathic pain.
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Rapid and effective treatment of cancer-induced bone pain remains a clinical challenge and patients with bone metastasis are more likely to experience severe pain. The voltage-gated sodium channel Nav1.8 plays a critical role in many aspects of nociceptor function. Therefore, we characterized a rat model of cancer pain and investigated the potential role of Nav1.8. ⋯ These findings suggest that Nav1.8 plays a role in the development and maintenance of bone cancer pain.