Pain
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The intensity of experimental pain is known to be dependent on stimulation duration. However, it remains unknown whether this effect arises largely from the actual stimulus duration or is substantially influenced by the subject's perception of the stimulus duration. In the present study, we questioned this issue by misleading the perception of the duration of pain in a population of 36 healthy volunteers stimulated with a thermode. ⋯ Although the intensity and the real duration of stimulation were identical in both conditions, the intensity of pain was significantly reduced when the perception of time was misleadingly shortened by the manipulated clock. This study suggests that the perceived duration of a noxious stimulation may influence the perceived intensity of pain. The perceived duration of the length of a noxious stimulation influences (decreases) the intensity of perceived pain.
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Migraine headache is one of the most common neurological disorders. The pathological conditions that directly initiate afferent pain signaling are poorly understood. In trigeminal neurons retrogradely labeled from the cranial meninges, we have recorded pH-evoked currents using whole-cell patch-clamp electrophysiology. ⋯ The desensitization time constant of pH 6.0-evoked currents in the majority of dural afferents was less than 500ms which is consistent with that reported for ASIC3 homomeric or heteromeric channels. Finally, application of pH 5.0 synthetic-interstitial fluid to the dura produced significant decreases in facial and hind-paw withdrawal threshold, an effect blocked by amiloride but not TRPV1 antagonists, suggesting that ASIC activation produces migraine-related behavior in vivo. These data provide a cellular mechanism by which decreased pH in the meninges following ischemic or inflammatory events directly excites afferent pain-sensing neurons potentially contributing to migraine headache.
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Oxaliplatin (OXAL) is a platinum-based drug used for the treatment of colorectal, lung, breast and ovarian cancers. OXAL does not cause renal or hematologic toxicity. However, OXAL induces neuropathic pain which hampers the chemotherapy success. ⋯ Furthermore, immunohistochemistry and confocal microscopic quantifications demonstrated that 3α,5α-THP repaired OXAL-induced neurochemical/cellular alterations by restoring IENF control density and normal level of neurofilament 200kDa that was strongly repressed by OXAL in dorsal root ganglion neurons and sciatic nerve axons. OXAL showed no toxicity for the non-compact myelin protein 2',3'-cyclic-nucleotide-3'-phosphodiesterase whose expression level was similarly increased by 3α,5α-THP in controls and OXAL-treated rat nerves. Together, these results may be interesting for the development of natural or safe neurosteroid-based neuroprotective strategy against anticancer drug-evoked painful neuropathy.