Articles: hyperalgesia.
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Proc. Natl. Acad. Sci. U.S.A. · Nov 2009
Activation of TRPV1 in the spinal cord by oxidized linoleic acid metabolites contributes to inflammatory hyperalgesia.
Transient receptor potential vanilloid 1 (TRPV1) plays a major role in hyperalgesia and allodynia and is expressed both in the peripheral and central nervous systems (CNS). However, few studies have evaluated mechanisms by which CNS TRPV1 mediates hyperalgesia and allodynia after injury. We hypothesized that activation of spinal cord systems releases endogenous TRPV1 agonists that evoke the development of mechanical allodynia by this receptor. ⋯ Finally, intrathecal neutralization of 9- and 13-HODE by antibodies blocks CFA-evoked mechanical allodynia. These data collectively reveal a mechanism by which an endogenous family of lipids activates TRPV1 in the spinal cord, leading to the development of inflammatory hyperalgesia. These findings may integrate many pain disorders and provide an approach for developing analgesic drugs.
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Neurogastroenterol. Motil. · Nov 2009
5-HT 3 receptors mediate the time-dependent vagal afferent modulation of nociception during chronic food allergen-sensitized visceral hyperalgesia in rats.
Converging lines of evidence demonstrate a vagally mediated antinociceptive pathway in animals undergoing acute visceral insults, the contribution of this system to visceral pain following chronic noxious stimuli is unknown. 5-HT(3) receptor (5-HT(3)Rs) on spinal afferents are crucially involved in nociceptive processing, the role of 5-HT(3)Rs on vagal afferents is unclear. The aim of the present study was to determine the contribution of vagal afferents to visceral nociception in rats undergoing chronic luminal allergen stimulation and whether it involves vagal 5-HT(3)Rs. Sensitized rats received chicken egg albumin (EA, 1 mg mL(-1)) in drinking water for 2 weeks (day 1-14). ⋯ Intraluminal infusion of a 5-HT(3)R antagonist (granisetron), whether alone or infused after local mucosa anaesthetic with 1% lidocaine, mimicked the effects of vagotomy. The mRNA levels for 5-HT(3B) or 5-HT(3A) subunit in the NG showed an opposite time-course to that of visceral pain, which increased from day 2, then decreased gradually to levels lower than those of controls. Our results demonstrate a time-dependent vagal afferent modulation of chronic allergen-sensitized visceral hyperalgesia, which may involve a 5-HT(3)R pathway.
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Slow deep breathing has been proposed as an effective method to decrease pain. However, experimental studies conducted to validate this claim have not been carried out. ⋯ Slow deep breathing and HR biofeedback had analgesic effects and increased vagal cardiac activity. Distraction also produced analgesia; however, these effects were not accompanied by concomitant changes in cardiac activity. This suggests that the neurobiology underlying respiratory-induced analgesia and distraction are different. Clinical implications are discussed, as are the possible cardiorespiratory processes responsible for mediating breathing-induced analgesia.
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Morbid obesity may be accompanied by diabetes and painful diabetic neuropathy, a poorly understood condition that is manifested by mechanical or thermal allodynia and hyperalgesia. Recent studies have highlighted the importance of T-type calcium channels (T-channels) in peripheral nociception; therefore, our goal was to examine the function of these channels in the pathophysiology and development of painful diabetic neuropathy. ⋯ Our results indicate that pharmacological antagonism of T-channels is potentially an important novel therapeutic approach for the management of painful diabetic neuropathy.