Articles: hyperalgesia.
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Brain Res. Mol. Brain Res. · Mar 2001
Selective upregulation of the flip-flop splice variants of AMPA receptor subunits in the rat spinal cord after hindpaw inflammation.
Glutamate receptors are involved in spinal nociceptive transmission and the development of persistent inflammatory hyperalgesia. It is unclear, however, whether there are changes in glutamate receptor gene expression associated with tissue injury. In the present study, we used reverse transcription-polymerase chain reaction (RT-PCR) to examine the modulation of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor gene expression in the rat spinal cord by inflammation. ⋯ Immunocytochemical analysis of GluR1 and GluR2 subunits indicate that the protein translation products of these subunits were also increased in the spinal cord. These results demonstrate an increased expression of AMPA receptor subunits that correlates with the acute phase of CFA-induced inflammation and hyperalgesia. Selective changes in the expression of the flip-flop splice variants of the AMPA receptor suggest a reorganization of the composition of the AMPA receptor complex and its involvement in the development of inflammatory hyperalgesia.
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Comparative Study
Heat hyperalgesia following partial sciatic ligation in rats: interacting nature and nurture.
As in humans, levels of neuropathic pain produced by nerve injury are highly variable among animals. This variability was attributed to genetic and environmental factors. ⋯ We show that heat sensitivity of intact rats and levels of heat hyperalgesia of PSL-injured rats were highly variable across eight different rat strains and seven different diets. Thus, genetic and environmental variables interact in determination of levels of chronic neuropathic sensory disorders in rats.
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Neuroscience letters · Mar 2001
Differential antinociceptive effect of transcutaneous electrical stimulation on pain behavior sensitive or insensitive to phentolamine in neuropathic rats.
The effects of transcutaneous electrical stimulation and systemic injection of phentolamine, a non-specific alpha-adrenergic antagonist, on the behavioral signs of mechanical allodynia and cold hyperalgesia in rats with nerve injury were investigated. Mechanical allodynia and cold hyperalgesia were evaluated by measuring the paw withdrawal frequency (PWF) resulting from repetitive application of a von Frey hair and the paw lift duration (PLD) at a cold temperature, respectively. After a unilateral nerve injury, both PWF and PLD increased in the injured hind paw. ⋯ Naloxone reversed the LFHI-TES produced depression of PWF. Intraperitoneal administration of phentolamine depressed the injury-induced increased PLD without affecting the injury-induced increased PWF. Our results suggest that LFHI-TES, which activates the endogenous opioid systems, produces an antinociceptive effect that appears to be related to whether or not the pain is mediated by sympathetic activity.
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The firing of neurones in spinal segments adjacent to a contusive T13 spinal cord injury was characterised in anaesthetised rats. Three groups of rats were examined: (1) allodynic spinally injured, (2) non-allodynic spinally injured and (3) normal, uninjured. Spinal cord field potentials evoked by electrical dorsal root stimulation and the responses of 207 dorsal horn neurones to mechanical stimuli applied to the skin were studied. ⋯ These changes were observed both rostral and caudal to the site of injury. The results suggest that an increased responsiveness of some dorsal horn neurones in segments neighbouring a contusive spinal cord injury may contribute to the expression of mechanical allodynia. It is proposed that a relative lack of inhibition underlies altered cell responses.
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Randomized Controlled Trial Clinical Trial
Concentration-effect relationship of intravenous alfentanil and ketamine on peripheral neurosensory thresholds, allodynia and hyperalgesia of neuropathic pain.
Both mu opioid agonists and N-methyl-D-aspartate (NMDA) receptor antagonists are implicated in the regulation of neuropathic pain in post-nerve injury preclinical pain models. This study characterizes the effects of intravenously infused alfentanil (a mu-receptor agonist) and ketamine (an NMDA-receptor antagonist) on human neuropathic pain states, characterized by allodynia and hyperalgesia. Using diphenhydramine as the placebo, alfentanil and ketamine infusions were given in a randomized double-blind fashion 1 week apart via a computer-controlled infusion (CCI) pump that was programmed to target plasma levels of alfentanil at 25, 50 and 75 ng/ml and ketamine at 50, 100 and 150 ng/ml. ⋯ Therefore, clinical utilization of opioids with careful titration may be beneficial in post-nerve injury patients with partial deafferentation. With the absence of significant CNS side effects, the ketamine infusion not only demonstrated the well-documented spinal cord mechanism of the NMDA receptor, but the result of the current study also suggests that a peripheral mechanism of NMDA receptor may exist. The relationship between central sensitization and regulation of peripheral NMDA-receptor expression requires further investigation.