Articles: hyperalgesia.
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Neuroscience letters · Jul 2012
Mechanisms of Bv8-induced biphasic hyperalgesia: increased excitatory transmitter release and expression.
Bv8 is a pronociceptive peptide that binds to two G-protein coupled prokineticin receptors, PK-R1 and PK-R2. These receptors are localized in the dorsal horn of the spinal cord and dorsal root ganglia (DRG) of nociceptive neurons in rodents. Systemic administration of Bv8 elicits a biphasic reduction in nociceptive thresholds to thermal and mechanical stimuli. ⋯ These data suggest that Bv8 induces hyperalgesia by direct release of excitatory transmitters in the spinal cord, consistent with the first phase of hyperalgesia. Additionally, Bv8 elicits a subsequent, protein-synthesis dependent increase in expression and release of excitatory transmitters that may underlie the long-lasting second phase of hyperalgesia. Activation of prokineticin receptors may therefore contribute to persistent hyperalgesia occurring as a consequence of tissue injury further suggesting that these receptors are attractive targets for development of therapeutics for pain treatment.
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Neurogastroenterol. Motil. · Jul 2012
Randomized Controlled TrialThe autonomic response to human esophageal acidification and the development of hyperalgesia.
Distal esophageal acidification induces variable hyperalgesia in the non-acid exposed proximal esophagus. As the autonomic nervous system (ANS) modulates nociception, the aim was to determine whether autonomic reactivity to acid infusion predicted inter-individual differences in hyperalgesia. ⋯ Acid-induced esophageal hyperalgesia correlated with reduced parasympathetic tone, suggesting that the parasympathetic nervous system may have anti hyperalgesic properties. Additional studies on the autonomic modulation of esophageal hyperalgesia are required.
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The transient receptor potential ankyrin 1 (TRPA1) ion channel is expressed on nociceptive primary afferent nerve fibers. On the distal ending, it is involved in transduction of noxious stimuli, and on the proximal ending (within the spinal dorsal horn), it regulates transmission of nociceptive signals. Here we studied whether the cutaneous or spinal TRPA1 ion channel contributes to mechanical hypersensitivity or guarding, an index of spontaneous pain, in an experimental model of postoperative pain in the rat. ⋯ The TRPA1 channel in the skin contributes to sustained as well noxious mechanical stimulus-evoked postoperative pain, whereas the spinal TRPA1 channel contributes predominantly to innocuous mechanical stimulus-evoked postoperative pain.
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Controlled Clinical Trial
Increased contact heat pain and shortened latencies of contact heat evoked potentials following capsaicin-induced heat hyperalgesia.
To examine changes in contact heat evoked potentials (CHEPs) and perceived pain intensity following acute sensitization with topical capsaicin. ⋯ Contact heat may be a useful tool to assess sensitization of the pain system.
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Anesthesia and analgesia · Jul 2012
Comparative StudyThe efficacy of morphine, pregabalin, gabapentin, and duloxetine on mechanical allodynia is different from that on neuroma pain in the rat neuropathic pain model.
It has been reported that <50% of neuropathic pain patients are satisfactorily treated with drugs. It is possible that this lack of efficacy of drugs on neuropathic pain might be due to the drugs prescribed, regardless of the origin of pain. We compared the efficacy of orally administered morphine, pregabalin, gabapentin, and duloxetine on mechanical allodynia with that on neuroma pain using the tibial neuroma transposition (TNT) model. ⋯ These data indicate that the potency of morphine and the efficacy of pregabalin, gabapentin, and duloxetine on mechanical allodynia are different from those on neuroma pain and that combination therapy is one of different therapeutic choices for the treatment of neuropathic pain.