Articles: hyperalgesia.
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Hua Xi Kou Qiang Yi Xue Za Zhi · Jun 2008
[Study of the influence of emotion stress on mechanical hyperalgesia of masseter muscles in rats].
To study the influence of emotion stress on mechanical hyperalgesia of masseter muscles in rats through the equipment of communication box. ⋯ It is suggested that emotion stress can lead to the hyperalgesia of masseter muscles and antidepressant drug can lower the hyperalgsia resulted of emotion stress.
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We describe the characterization of a partial saphenous nerve injury (PSNI) model of neuropathic pain in the mouse. PSNI resulted in significant mechanical allodynia in mice with no behavioural change to temperature stimulation. ⋯ In galanin knockout mice, PSNI failed to induce allodynia as previously reported in other neuropathic pain models. PSNI can be used to simultaneously study behavioural and neurophysiological changes in wild-type and transgenic mice.
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The contralateral pain-related behavioral and immunohistochemical changes after hemilateral spinal nerve injury in rats were investigated. ⋯ These results suggest that contralateral mechanical allodynia induced by hemilateral spinal nerve injury is associated with upregulation of satellite cells and TNF-alpha in the contralateral DRG. In addition, our results suggest that spinal astrocytes play an important role in these contralateral changes.
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We determined if cutaneous hyperalgesia and pain-induced c-Fos overexpression in the spinal cord produced by repeated forced swimming (FS) stress in the rat were related to changes in GABA neurotransmission by studying spinal release of GABA and the effect of positive modulation of GABA-A receptors with diazepam. Male rats were daily submitted to 10-20 min of either forced swimming or sham swimming (SS) for 3 consecutive days. Two days later, spinal GABA release was estimated by in vivo microdialysis. ⋯ In FS rats, diazepam did not have effect on GABA release but reduced pain scores and overexpression of c-Fos whereas flumazenil (0.1 mg/kg, i.p.), an antagonist of the benzodiazepine binding site, reversed these effects. When diazepam was given only 1h before the formalin test, it slightly but significantly reduced pain scores during late phase in FS rats but not in SS rats. In conclusion, stress-induced reduction in GABA-A receptor activation is involved in the development of FS stress-induced hyperalgesia.
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Subcutaneous formalin injection has been used extensively to evaluate acute effects (over several hours) of chemical nociceptive stimulation on nociceptive reflexes. Also, a persistent hyperreflexia for mechanical and thermal stimulation, lasting 3 weeks after formalin injection, has been revealed and related to microglial activation in the spinal dorsal horn. The present study demonstrates more prolonged effects of formalin injection, lasting 6 weeks, on operant escape from nociceptive thermal stimulation. ⋯ Normal reductions in skin temperature during thermal stimulation were attenuated (nearly eliminated) at 1 and 2 weeks after formalin injection and partially recovered by 10 weeks. Thus, formalin-induced tissue injury produced a long-term secondary hyperalgesia, accompanied by a reduced sympathetic responsivity. The similar time-course for these phenomena suggests that there are mechanistic linkages between focal injury, autonomic dysregulation and enhanced pain sensitivity.