Articles: hyperalgesia.
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Spinal cord injury (SCI) induces incapacitating neuropathic pain in the form of allodynia-a painful response to normally non-noxious stimuli. Unfortunately, the underlying mechanisms of these sensory changes are not well understood, and effective treatments for allodynia have proven elusive. We examined whether physical exercise can improve sensory function after experimental SCI by promoting neurotrophin expression in the spinal cord and periphery, which modulates synaptic transmission and function. ⋯ No other exercise paradigm restored BDNF centrally and peripherally. Greater recovery from allodynia correlated significantly with the degree of normalization of central and peripheral BDNF levels. These findings suggest that rhythmic, weight-bearing exercise may be an effective intervention to counter SCI-induced allodynia.
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The present study investigated whether mechanical allodynia following contusive spinal cord injury (SCI) of the thoracic segments 12 and 13 of the rat was associated with a reduction in gamma-aminobutyric acid (GABA)ergic inhibition adjacent to the site of injury. Five to 7 days following SCI, extracellular recordings were obtained from dorsal horn neurones located 1-2 segments caudal to the injury, in non-allodynic and allodynic halothane anaesthetised rats and from comparable neurones in normal rats. To assess spinal GABAergic inhibition in the three groups of animals, spontaneous and evoked cell firing rates were recorded before, during and after microiontophoretic application of the GABA(A) receptor antagonist bicuculline. ⋯ In non-allodynic SCI animals, bicuculline ejection led to significant changes in receptive field size, paired-pulse depression and responses to brush and pinch stimulation that were comparable to those observed in normal animals. By contrast, in allodynic SCI animals, bicuculline ejection had little or no effect on dorsal horn neurone responses to mechanical skin stimuli and paired-pulse depression despite reliably blocking the inhibition of cell firing produced by similarly applied GABA. The demonstration of reduced GABAergic inhibition predominantly in the allodynic SCI rats suggests that such a deficiency contributed to this pain-related behaviour acutely following SCI.
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Neuroscience letters · May 2004
Comparative StudyLocomotor recovery and mechanical hyperalgesia following spinal cord injury depend on age at time of injury in rat.
We tested the effect of age at the time of spinal cord injury (SCI) on locomotor recovery, in open field tests, and mechanical hyperalgesia, using paw withdrawal frequency (PWF) in response to noxious mechanical stimuli, in male Sprague-Dawley rats after spinal hemisection at T13 in young (40 days), adult (60 days) and middle-age (1 year) groups. Behavioral outcomes were measured weekly for 4 weeks in both SCI and sham groups. ⋯ The PWF of the young group was significantly increased, the adult group was significantly decreased, and the middle-age group showed no significant change in fore- and hindlimbs when compared to other age groups, pre-injury and sham controls. These results support age-dependent behavioral outcomes after SCI.
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Neuroscience letters · May 2004
Peripheral and electrocortical responses to painful and non-painful stimulation in chronic pain patients, tension headache patients and healthy controls.
Sixteen chronic back pain (CBP) patients, 16 tension headache (THA) patients and 16 healthy controls (HC) were exposed to four series of ten electric stimuli at perception threshold, pain threshold and 10% below pain tolerance. The EEG was recorded from three sites, in addition, the EMG from the m. frontalis and m. erector spinae, heart rate and skin conductance were assessed. The CBP patients showed significantly lower pain threshold and pain tolerance values than the HC and the THA patients whereas the THA patients displayed a higher pain tolerance. ⋯ N150, P260, P300 and N500 were not significantly different between the groups nor were there significant group differences in the peripheral measures. However, since the stimulation intensity was significantly lower in the CBP patients, these data are indicative of both enhanced central and peripheral reactivity. The observed lack of habituation may contribute to the persistence of chronic pain.
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Inflammatory proteases (mast cell tryptase and trypsins) cleave protease-activated receptor 2 (PAR2) on spinal afferent neurons and cause persistent inflammation and hyperalgesia by unknown mechanisms. We determined whether transient receptor potential vanilloid receptor 1 (TRPV1), a cation channel activated by capsaicin, protons, and noxious heat, mediates PAR2-induced hyperalgesia. PAR2 was coexpressed with TRPV1 in small- to medium-diameter neurons of the dorsal root ganglia (DRG), as determined by immunofluorescence. ⋯ PAR2 activation also potentiated capsaicin-induced release of substance P and calcitonin gene-related peptide from superfused segments of the dorsal horn of the spinal cord, where they mediate hyperalgesia. We have identified a novel mechanism by which proteases that activate PAR2 sensitize TRPV1 through PKC. Antagonism of PAR2, TRPV1, or PKC may abrogate protease-induced thermal hyperalgesia.