Pain
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This study tested the hypothesis that fibromyalgia patients display hypervigilance for somatosensory signals. Hypervigilance was operationalized as the detection of weak electrocutaneous stimuli. Innocuous electrical stimuli gradually increasing in strength were administered to one of four different body locations. ⋯ No evidence for hypervigilance for innocuous signals was found: patients did not show superior detection of electrical stimuli either under single or dual task conditions. Also, no differences were found between patients and controls on the body vigilance questionnaire. Detection of electrical stimuli was, however, predicted by pain-related fear and pain vigilance.
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Although intrathecal administration of baclofen, a selective GABA(B)-receptor agonist, is known to have an antinociceptive effect on various pain models, the role of presynaptic GABA(B) receptors in antinociception is not well characterized. In the present study, the action of baclofen on primary afferent-evoked glutamatergic excitatory transmission was examined in substantia gelatinosa (SG) neurons of an adult rat spinal cord slice with an attached dorsal root, prepared from the lumbar segment, by use of the blind whole-cell patch-clamp technique. Under the condition where a postsynaptic action of baclofen was inhibited, baclofen (1 microM) reduced the amplitudes of excitatory postsynaptic currents (EPSCs; V(H)=-70 mV) which were monosynaptically evoked by stimulating primary-afferent C- and/or Adelta-fibers and which were remarkably depressed by CNQX (10 microM). ⋯ Baclofen (1 microM) did not affect a response of SG neurons to bath-applied AMPA (10 microM). These results indicate that baclofen inhibits the release of L-glutamate from Adelta and C primary-afferent terminals in the SG through the activation of GABA(B) receptor; this action is more effective to C-fiber than Adelta-fiber transmission. Considering that the SG is the main part of termination of Adelta- and C-fibers transmitting nociceptive information, the present finding would account for at least a part of the inhibitory action of baclofen on pain transmission.
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We examined the role of B1 and B2 bradykinin receptors in promoting neuropathic hypersensitivity following peripheral nerve injury. Forty eight-hours following chronic constriction injury to a rat sciatic nerve there was an increased expression of B2 receptor mRNA in the lumbar dorsal root ganglia ipsilateral to the site of nerve injury. ⋯ While HOE-140, a potent B2 receptor antagonist was analgesic at both time points tested, the B1 receptor antagonist des-Arg(9), [Leu(8)]-BK had an analgesic effect only at 14 days. The results support the concept that peripheral nerve injury is associated with local inflammation and that bradykinin, acting on both of its receptors promotes pain hypersensitivity.