Articles: hyperalgesia.
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Comparative Study
Blockade of sensory abnormalities and kinin B(1) receptor expression by N-acetyl-L-cysteine and ramipril in a rat model of insulin resistance.
Glucose-fed rat is a model of insulin resistance that displays sensory polyneuropathy and hypertension. This study aimed at comparing the beneficial effects of N-acetyl-L-cysteine (NAC, antioxidant) and ramipril (angiotensin-1 converting enzyme inhibitor) on tactile and cold allodynia induced by chronic glucose feeding. Impact of these treatments was also assessed on hypertension, plasma glucose and insulin concentrations, insulin resistance and kinin B(1) receptor expression. ⋯ High systolic blood pressure, hyperinsulinemia, insulin resistance and kinin B(1) receptor expression were also normalized or attenuated in glucose-fed rats by either treatment. Results suggest that chronic treatment with an antioxidant or an ACE inhibitor provides similar beneficial effects on sensory polyneuropathy, hypertension and insulin resistance in glucose-fed rats. Both therapies were associated with a reduction of the expression of the pro-nociceptive kinin B(1) receptor.
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Neuroscience letters · Jul 2008
Activation of spinal microglia in a murine model of peripheral inflammation-induced, long-lasting contralateral allodynia.
Increased sensitivity contralateral to an injury has been described in humans and in various models of neuropathic pain in rats. The mechanism underlying contralateral hypersensitivity is as yet unclear, although previous studies have implicated involvement of both spinal neurons and glia. ⋯ The delayed development of contralateral allodynia correlated with an increase in OX-42, but not GFAP immunoreactivity in the contralateral dorsal horn. Furthermore, intrathecal treatment with minocycline inhibited the development of contralateral allodynia, suggesting that microglial activation plays a key role in contralateralization, and may be a potential target for clinical intervention after injury or inflammation has occurred, to eliminate the subsequent development of extraterritorial pain.
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It has been shown that interleukin-1beta (IL-1beta) facilitates nociception during neuropathic and inflammatory pain, but its involvement in bone cancer pain and its mechanisms have not previously been established. This study is an investigation of IL-1beta spinal expression and the N-methyl-D-aspartate (NMDA) receptor (NMDAR) NR1 subunit phosphorylation during cancer pain, co-localization of IL-1 receptor type I (IL-1RI) and NMDAR in the spinal cord, and the effects of IL-1 receptor antagonist (IL-1ra) on NMDAR1 (NR1) phosphorylation and hyperalgesia in a rat model of bone cancer pain. Cancer was induced by injecting AT-3.1 prostate cancer cells into the tibia of the male Copenhagen rat. ⋯ Spinal cords were removed for Western blot to measure IL-1beta and NR1 phosphorylation and for double immunostaining of IL-1RI and NR1. The data showed that 1) spinal IL-1beta was up-regulated and NR1 phosphorylation was increased, 2) IL-1ra at 0.1 mg/rat significantly (P<0.05) inhibited mechanical hyperalgesia, increasing PWPT on day 14 from 71.1+/-3.1-85.3+/-4.6 g and on day 19 from 73.5.0+/-3.5-87.1+/-3.7 g, and inhibited NR1 phosphorylation compared with saline control, and 3) IL-1RI is localized in NR1-immunoreactive neurons within the spinal cord. The results suggest that spinal IL-1beta enhances NR1 phosphorylation to facilitate bone cancer pain.
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Idiopathic chronic pain conditions with a mismatch between anatomical abnormalities and symptoms can be categorized as somatoform pain disorder according to the DSM-IV criteria. A dysfunction of pain processing circuits has been suggested as one underlying pathophysiological factor. There is accumulating evidence for a crucial role of affect regulating brain structures such as the medial frontal cortex in this context. ⋯ The average ratings for experimentally induced pain were not significantly different between controls and patients concerning pain intensity and pain unpleasantness. Comparing patients with controls a pain related hypoactive state of the ventromedial prefrontal/orbitofrontal cortex (BA 10/11) and a hyperactive state of the parahippocampal gyrus, amygdala and anterior insula were found in the patient group. Our findings of an altered cerebral processing of experimentally induced pain in patients with somatoform pain disorder support the hypothesis of dysfunctional pain processing, especially in affect regulating regions.
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This study examined within- and across-session consistency of visual analog scale (VAS) pain intensity and unpleasantness ratings of contact heat stimuli in 64 subjects (32 male). Subjects participated in four sessions over 14 days, with three stimulus series per session. Two levels of painful heat (pain-lo: rated 40, and pain-hi: rated 70 on a 0-100 VAS) were delivered in randomized order during each series, with temperatures selected on an individual subject basis to equalize pain perception across subjects. ⋯ Across- and within-session CVs were significantly negatively correlated with individual ratings of the stimuli, but were not correlated with demographic or psychosocial factors. Furthermore, sex did not impact consistency of ratings, demonstrating that neither sex is more variable in ratings than the other over time. Taken together, these findings suggest that VAS ratings of painful contact heat are relatively stable over time but the variability of these ratings is significantly impacted by the perceived intensity of the stimulus.