Articles: hyperalgesia.
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B vitamins can effectively attenuate inflammatory and neuropathic pain in experimental animals, while their efficacy in treating clinical pain syndromes remains unclear. To understand possible mechanisms underlying B vitamin-induced analgesia and provide further evidence that may support the clinical utility of B vitamins in chronic pain treatment, this study investigated effects of thiamine (B1) on the excitability and Na currents of dorsal root ganglion (DRG) neurons that have been altered by nerve injury. ⋯ Thiamine can reduce hyperexcitability and lessen alterations of Na currents in injured DRG neurons, in addition to suppressing thermal hyperalgesia.
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Intraplantar injection of bee venom (BV) produces persistent spontaneous nociception (PSN) and hyperalgesia, as well as obvious inflammatory swelling, in the paws of injected rats. The present study was designed to determine the peripheral roles of mitogen-activated protein kinase (MAPK) signal transduction pathways in BV-induced nociception and inflammation. We examined the effect of intraplantar injection of an ERK1/2 inhibitor, PD98059, and a p38 inhibitor, SB202190, on BV-induced PSN, mechanical hyperalgesia, and inflammatory swelling. We found that (1) pretreatment with SB202190 (0.1 to 10 microg) had no effect on BV-induced PSN, whereas pretreatment with PD98059 (0.1 to 100 microg) produced a significant and dose-dependent inhibition of BV-induced PSN; (2) pretreatment with PD98059 (0.1 to 100 microg) had no effect on BV-induced decreases in paw withdrawal mechanical threshold (PWMT), while pretreatment with SB202190 (0.1 to 10 microg) produced an obvious prevention of the BV-induced decrease in PWMT; and (3) pretreatment with PD98059 (0.1 to 100 microg) had no effect on BV-induced increase in paw volume (PV), whereas pretreatment with SB202190 (0.1 to 10 microg) produced a dose-related inhibition of BV-induced increases in PV. No contralateral drug treatments, even at the highest dose, had any effect on BV-induced PSN, PWMT or PV, ruling out the systemic effect of these drugs. These results suggest that peripheral MAPK signal transduction pathways may play differential roles in bee venom-induced nociception and inflammation. Targeting specific peripheral MAPKs might prove effective in the treatment of persistent pain and inflammation. ⋯ The present article showed that intraplantar injection of different MAPK inhibitors produced differential effects on bee venom-induced nociception and inflammation, suggesting that the peripheral MAPK signal transduction pathways have differential roles. Targeting specific peripheral MAPKs might prove effective in the treatment of persistent pain and inflammation.
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The aim of the study was to evaluate whether or not there exists nociceptive and non-nociceptive hypersensitivity at latent myofascial trigger points (MTrPs). ⋯ These results confirm the existence of nociceptive hypersensitivity at latent MTrPs and provide the first evidence that there exists non-nociceptive hypersensitivity (allodynia) at latent MTrPs. Finally, the occurrence of referred muscle pain is associated with higher pain sensitivity at latent MTrPs.
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Annals of neurology · Feb 2009
beta(2)-adrenoceptors are critical for antidepressant treatment of neuropathic pain.
Tricyclic antidepressants (TCAs) are one of the first-line pharmacological treatments against neuropathic pain. TCAs increase the extracellular concentrations of noradrenaline and serotonin by blocking the reuptake transporters of these amines. However, the precise downstream mechanism leading to the therapeutic action remains identified. In this work, we evaluated the role of adrenergic receptors (ARs) in the action of TCAs. ⋯ Stimulation of beta(2)-AR is necessary for nortriptyline to exert its antiallodynic action against neuropathic pain. These findings provide new insight into the mechanism by which antidepressants alleviate neuropathic pain. Our results also raise the question of a potential incompatibility between beta-blockers that affect beta(2)-AR and antidepressant drugs in patients treated for neuropathic pain.
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Increasing evidence suggests that chronic stress plays an important role in the pathophysiology of several functional gastrointestinal disorders. We investigated whether cannabinoid receptor 1 (CB1) and vanilloid receptor 1 (TRPV1; transient receptor potential vanilloid 1) are involved in stress-induced visceral hyperalgesia. ⋯ These results suggest that the endocannabinoid (CB1) and TRP (TRPV1) pathways may play a potentially important role in stress-induced visceral hyperalgesia.