Articles: hyperalgesia.
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Physical therapists frequently use joint mobilization therapy techniques to treat people with musculoskeletal dysfunction and pain. Several studies suggest that endogenous adenosine may act in an analgesic fashion in various pain states. ⋯ This study demonstrated the involvement of the adenosinergic system in the antihyperalgesic effect of AJM in a rodent model of pain and provides a possible mechanism basis for AJM-induced relief of acute pain.
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Besides stimulating angiogenesis or cell survival, basic fibroblast growth factor (bFGF) has the potential for protecting neurons in the injured spinal cord. ⋯ Our findings suggest that bFGF-incorporated GH could have therapeutic potential for alleviating mechanical allodynia following spinal cord injury.
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In rodents, surgery and/or remifentanil induce postoperative pain hypersensitivity together with glial cell activation. The same stimulus also produces long-lasting adaptative changes resulting in latent pain sensitization, substantiated after naloxone administration. Glial contribution to postoperative latent sensitization is unknown. ⋯ A transient microglia/macrophage and astrocyte activation was present between 30 min and 2 days postoperatively, while increased immunoreactivity in satellite glial cells lasted 21 days. At this time point, (-) naloxone, but not (+) naloxone, increased GFAP in satellite glial cells; conversely, both naloxone steroisomers similarly increased GFAP in the spinal cord. The report shows for the first time that surgery induces long-lasting morphological changes in astrocytes and satellite cells, involving opioid and toll-like receptors, that could contribute to the development of latent pain sensitization in mice.
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Mechanical dynamic allodynia is a hallmark symptom of postherpetic neuralgia, but the mechanisms are unclear. This study examined the participation of injury to sensory C-fiber and A-fiber neurons in postherpetic dynamic allodynia. Percutaneous inoculation of mice with herpes simplex virus type-1 caused zoster-like skin lesions and dynamic allodynia, which persisted after lesion healed. ⋯ Calcitonin gene-related peptide immunoreactivity (a C-fiber marker) was markedly reduced, but neurofilament 200 immunoreactivity (an A-fiber neuron marker) was unchanged in the scarred skin of postherpetic mice. In the affected dorsal root ganglion of postherpetic mice, peripherin-immunoreactive (a C-fiber neuron marker) neurons reduced significantly, whereas neurofilament 200-immunoreactive neurons did not. These results suggest that postherpetic dynamic allodynia is associated with injury to sensory C-fiber neurons and little damage to A-fiber neurons.