Articles: hyperalgesia.
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Nuclear factor-kappa B (NF-kappaB) is a gene transcriptional regulator of inflammatory cytokines. We investigated the transduction efficiency of NF-kappaB decoy to dorsal root ganglion (DRG), as well as the decrease in nerve injury, mechanical allodynia, and thermal hyperalgesia in a rat lumbar disc herniation model. Forty rats were used in this study. ⋯ Mechanical allodynia and thermal hyperalgesia were significantly suppressed in the herniation + decoy group. NF-kappaB decoy was transduced into DRGs in vivo. NF-kappaB decoy may be useful as a target for clarifying the mechanism of sciatica caused by lumbar disc herniation.
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We evaluated the effects of haloperidol and its metabolites on capsaicin-induced mechanical hypersensitivity (allodynia) and on nociceptive pain induced by punctate mechanical stimuli in mice. ⋯ These results show that haloperidol and its metabolites I and II produce antiallodynic but not antinociceptive effects against punctate mechanical stimuli and suggest that their antiallodynic effect may be due to blockade of sigma(1) receptors but not to dopamine receptor antagonism.
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Central neuroimmune activation contributes to the initiation and maintenance of neuropathic pain after nerve injury. The current study was aimed to examine the modulation of neuroimmune activation in the spinal cord by the alpha(2) adrenoceptor agonist, clonidine, in a rat model of neuropathic pain induced by partial sciatic nerve ligation (PSNL). Animals were randomly assigned into 6 groups: sham-operation with 20 microg clonidine or saline; and PSNL with clonidine (5, 10, and 20 microg) or saline. ⋯ Administration of clonidine resulted in a dose-dependent attenuation in PSNL-induced mechanical and thermal hyperalgesia. Furthermore, clonidine could markedly inhibit neuroimmune activation characterized by glial activation, production of cytokines, NF-kappaB activation as well as p38 activation. The antihyperalgesic effect of intrathecal clonidine in rats receiving PSNL might partly attribute to the inhibition of neuroimmune activation associated with the maintenance of neuropathic pain.
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Despite the clear roles played by peroxisome proliferators-activated receptor alpha (PPAR-alpha) in lipid metabolism, inflammation and feeding, the effects of its activation in the central nervous system (CNS) are largely unknown. Palmitoylethanolamide (PEA), a member of the fatty-acid ethanolamide family, acts peripherally as an endogenous PPAR-alpha agonist, exerting analgesic and anti-inflammatory effects. Both PPAR-alpha and PEA are present in the CNS, but the specific functions of this lipid and its receptor remain to be clarified. ⋯ To investigate the mechanism by which PEA attenuated hyperalgesia, we evaluated inhibitory kB-alpha (IkB-alpha) degradation and p65 nuclear factor kB (NF-kappaB) activation in DRG. PEA prevented IkB-alpha degradation and p65 NF-kappaB nuclear translocation, confirming the involvement of this transcriptional factor in the control of peripheral hyperalgesia. These results add further support to the broad-spectrum of biological and pharmacological effects induced by PPAR-alpha agonists, suggesting a centrally mediated component for these drugs in controlling inflammatory pain.
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Prog. Neuropsychopharmacol. Biol. Psychiatry · Jun 2009
Intracisternal administration of COX inhibitors attenuates mechanical allodynia following compression of the trigeminal ganglion in rats.
The purpose of the present study was to investigate the role of central cyclooxygenase (COX) pathways in the modulation of mechanical allodynia following compression of the left trigeminal ganglion. Experiments were carried out on male Sprague-Dawley rats mounted onto a stereotaxic frame under anesthesia. For compression, a 4% agar solution (10 microl) was injected into the trigeminal ganglion. ⋯ Intracisternal administration of indomethacin, a non-selective COX inhibitor, SC-560, a selective COX-1 inhibitor, or NS-398, a selective COX-2 inhibitor, significantly inhibited mechanical allodynia. The individual anti-allodynic effects of the three COX inhibitors persisted for 6 h and returned to pretreatment values within 24 h. Based on these results, the blockade of central COX pathways may comprise a potential new therapeutic tool for the treatment of trigeminal ganglion compression-induced nociception.