Articles: hyperalgesia.
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CART peptides are found in brain and spinal cord areas involved in pain transmission. In the present study, we investigated the role of rat CART (55-102) in the modulation of chronic pain using models of chronic neuropathic (nerve injury model) and inflammatory (carrageenan test) pain models in the mouse after intrathecal administration. ⋯ Although CART (55-102) attenuated carrageenan-induced hyperalgesia, it failed to reduce the inflammation associated with this model. These results suggest the involvement of the CART peptides in the development of hyperalgesia and allodynia associated with neuropathic pain.
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Neuroscience research · Aug 2006
The lumbar spinal cord glial cells actively modulate subcutaneous formalin induced hyperalgesia in the rat.
We investigated the response and relationship of glial cells and neurons in lumbar spinal cord to hyperalgesia induced by the unilateral subcutaneous formalin injection into the hindpaw of rats. It was demonstrated that Fos/NeuN immunoreactive (-IR) neurons, glial fibrillary acidic protein (GFAP)-IR astrocytes and OX42-IR microglia were distributed in dorsal horn of lumbar spinal cord, predominantly in the superficial layer. In the time-course studies, GFAP-IR astrocytes were firstly detected, OX42-IR microglia were sequentially observed, Fos/NeuN-IR neurons were found slightly late. ⋯ Ninety-one HGJs were found in 100 areas of experimental rats and occupied 91%, while only 39% HGJs were found in control rats. In experimental rats pretreated with intrathecal (i.t.) application of the carbenoxolone (a gap junction blocker) or fluorocitrate (a glial metabolic inhibitor), the paw withdrawal thermal latency was prolonged than those application of the sterile saline (i.t.). It suggests that spinal cord glial cells may play an important role for modulation of hyperalgesia induced by noxious stimuli through HGJs which located between astrocytes and neurons.
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J. Neurosci. Methods · Jul 2006
Characterization of hind paw licking and lifting to noxious radiant heat in the rat with and without chronic inflammation.
The paw withdrawal latency to thermal radiant heat stimuli is a widely used nociceptive measure to study hyperalgesic mechanisms. In the present study, in addition to the paw withdrawal latency, two behavioral components of pain behaviors, paw licking and paw lifting have been characterized and quantified. The thermal stimuli were successively applied to the plantar surface of the rat hind paws and recorded the behavioral responses to each of the stimuli. ⋯ The paw withdrawal latency decreased in inflamed rats in comparison with control rats. These data informs that noxious radiant heat specifically evokes the frequency of paw lifting behavior in normal physiological condition, and paw licking behavior in a pathological inflammatory condition. These findings suggest that in addition to the measurement of PWL, scoring of paw licking and lifting behaviors will improve the sensitivity of this pain test.
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Hyperbaric oxygen therapy has been used to treat a variety of ailments from carbon monoxide poisoning to fibromyalgia. The purpose of this experiment was to explore the effect of hyperbaric oxygen treatment on carrageenan-induced inflammation and pain in rats. Hyperbaric oxygen treatment significantly decreased inflammation and pain following carrageenan injection. Clinically hyperbaric oxygen may be used in situations where NSAIDS are contraindicated or in persistent cases of inflammation.
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The susceptibility of changes in responsiveness to noxious cold stimulation of rats submitted to chronic constriction of the infraorbital nerve (CION) or carrageenan to drug inhibition was compared. Nocifensive responses were measured as total time rats engaged in bilateral facial grooming with both forepaws over the first 2 min following tetrafluoroethane spray application to the snout. Carrageenan (50 microg, s.c. into upper lip) caused short-lived ipsilateral cold hyperalgesia (peak at 3 h: vehicle 8.4+/-1.3, carrageenan 21.2+/-3.0 s) which was markedly suppressed by i.p. indomethacin (4 mg/kg), celecoxib (10mg/kg) or s.c. dexamethasone (0.5 mg/kg), endothelin ET(A) or ET(B) receptor antagonists (BQ-123 and BQ-788, respectively; 10 nmol/lip). ⋯ Bosentan (dual ET(A)/ET(B) receptor antagonist, 10 mg/kg, i.v.) abolished CION-induced cold hyperalgesia for up to 6h. Thus, once established, CION-induced orofacial hyperalgesia to cold stimuli appears to lack an inflammatory component, but is alleviated by endothelin ET(A) and/or ET(B) receptor antagonists. If this CION injury model bears predictive value to trigeminal neuralgia (i.e., paroxysmal orofacial pain triggered by various stimuli), endothelin receptors might constitute new targets for treatment of this disorder.