Pain
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Comparative Study
Possible impact of genetic differences on the development of neuropathic pain-like behaviors after unilateral sciatic nerve ischemic injury in rats.
The development of neuropathic-like behaviors following unilateral ischemic injury to the sciatic nerve was examined and compared in four rat strains: Sprague--Dawley (SD), Wistar--Kyoto (WK), spontaneously hypertensive (SHR) and Dark--Agouti (DA). We have also compared two sub-strains of SD rats supplied from two different vendors (SD-BK and SD-DK). The responses to mechanical, heat or cold stimuli of both hind paws were measured before and regularly after injury for up to 10 weeks. ⋯ The apparent resistance of DA rats to nerve ischemia, however, may suggest that genetic factors not directly related to pain modulation also play a role in the diverse outcomes. Our results indicate that sub-strains of rats also showed variable development of neuropathic pain-like behaviors to both the modality and magnitude of the effect. Thus, controlling sub-strains is also important in experimental studies of neuropathic pain in rats.
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The present study was designed to further characterize hypnotic analgesia and particularly to examine whether the effects are due to a selective alteration of pain perception and are organized somatotopically. Thirty-two healthy volunteers participated in this study. Thermal detection thresholds for warmth and cool stimuli and heat pain thresholds were measured at both the upper and lower left limbs by means of a thermotest. ⋯ Mean detection thresholds for warmth and cool stimuli were also altered at both the lower and upper limbs during hypnosis, but these modifications were correlated neither with susceptibility nor with the changes in heat pain threshold. These results indicate that hypnotic suggestions can selectively and somatotopically alter pain sensation in highly susceptible subjects. It is also suggested, however, that suggestions of analgesia can induce selective alterations of pain perception in poorly susceptible subjects, although these effects did not appear to be localized 'appropriately'.
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Peripheral inflammation induced with a knee joint injection of a mixture of kaolin/carrageenan (k/c) produces primary and secondary hyperalgesia. Inflammatory pain is thought to involve a variety of transmitters released from nerve terminals, including amino acids, substance P (SP) and calcitonin gene-related peptide (CGRP). In the present study, mice deficient in the calcitonin/alpha CGRP gene (CGRP(-/-)) displayed normal responses to noxious stimuli. ⋯ The CGRP(-/-) mice also had a prolonged rather than a shortened response latency in the hot-plate test 4 h after knee joint injection of k/c. Immunohistological study showed that CGRP-like immunoreactivity (CGRP-LI) was absent in the spinal cord and dorsal root ganglia taken from the CGRP(-/-) mice. These results indicate that endogenous CGRP plays an important role in the plastic neurogenic changes occurring in response to peripheral inflammatory events including the development of nociceptive behaviors.
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A growing body of evidence supports a nicotinic cholinergic approach to pain management, as neuronal nicotinic receptor agonists have shown efficacy across animal models of both inflammatory and neuropathic pain. However, most of these investigations have focused on the spinal system, and there is to date no report of nicotinic receptor-mediated antinociception in any pain model involving the trigeminal field of innervation. Thus, the purpose of the present studies was to evaluate whether the neuronal nicotinic receptor agonist epibatidine possesses antihyperalgesic activity in the formalin model of facial pain. ⋯ Finally, pretreatment with the selective neuronal nicotinic receptor antagonist mecamylamine completely abolished the antihyperalgesic effect of epibatidine in both phases. Taken together, these studies demonstrate that in both the acute and tonic phases of the formalin model of facial pain, epibatidine produces a neuronal nicotinic receptor-mediated antihyperalgesia that is both dose- and time-dependent. These results support the rationale for exploring the clinical efficacy of nicotinic agonists as analgesics to treat certain types of trigeminal pain in humans.
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A midline dorsal column lesion has been shown to be an effective surgical treatment for the relief of pelvic visceral pain in patients. The aim of this study was to examine the effectiveness of a dorsal column lesion upon: (i) increased electrophysiological responses of neurons in the ventral posterolateral thalamic nucleus in anesthetized rats evoked by the application of bradykinin to the surface of the pancreas, and (ii) pain-related behaviors observed after pancreatic infusion with bradykinin. In rats anesthetized with pentobarbital, recordings from individual thalamic neurons were made using tungsten electrodes. ⋯ A dorsal column lesion made prior (1 week) to the bradykinin infusion reduced the decrease in exploratory behavior but did not return exploratory behavior to control levels. In conclusion, nociceptive information relayed to the thalamus about the pancreas is transmitted from the spinal cord through the dorsal columns, possibly by the post-synaptic dorsal column pathway. However, the dorsal column pathway may not be the sole route for relaying information about noxious stimulation of the pancreas, particularly that impacting complex behavioral responses.