Neuroscience letters
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Neuroscience letters · Aug 2008
Randomized Controlled Trial Controlled Clinical TrialHeat pain threshold and tolerance show no left-right perceptual differences at complementary sites of the human forearm.
Pain threshold and pain tolerance of heat noxious stimuli were assessed to determine whether they are equivalent when measured at three equidistant sites of both volar forearms. Heat pain threshold and tolerance were measured in 18 healthy volunteers using a standard stimulation device consisting of a thermode. ⋯ This data completes previous reports on side effects by analyzing the effect of site on the forearm for both heat pain threshold and tolerance. The absence of side and site effects may contribute to setting a more secure basis for assessments of laterality effects of painful stimulation.
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Xenon and other inhalational agents induce cell and organ protection through different and only partially elucidated molecular mechanisms. Anesthesia induced or pharmacologic preconditioning is a recognized mechanism of cell protection. ⋯ ADNP was found to be differentially expressed by SSH, validated by Relative Real-Time PCR (RT-PCR) and confirmed by western blot and immunohistochemistry. The differential expression of ADNP in the rat neonatal brain may account for the preconditioning and neuroprotective effects exerted by gas xenon.
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Neuroscience letters · Aug 2008
Transient receptor potential ankyrin-1 participates in visceral hyperalgesia following experimental colitis.
Transient receptor potential ankyrin-1 (TRPA1) is an important receptor that contributes to inflammatory pain. However, previous studies were mainly concerned with its function in somatic hyperalgesia while few referred to visceral, especially colonic inflammatory hyperalgesia. The present study was aimed to investigate the role of TRPA1 in visceral hyperalgesia after trinitrobenzene sulfonic acid (TNBS)-induced colitis. ⋯ Intrathecal administration of TRPA1 antisense (AS) oligodeoxynucleotide (ODN) reduced the TRPA1 expression in DRG as well as suppressed the colitis-induced hyperalgesia to nociceptive colonic distension and intracolonic allyl isothiocyanate (AITC). Meanwhile the TRPA1 antisense ODN had no effect on transient receptor potential vanilloid-1 (TRPV1) expression, which was proposed to highly co-express with TRPA1, and no effect on the response to TRPV1 agonist, capsaicin. These data suggest an apparent role of TRPA1 in visceral hyperalgesia following colitis that might provide a novel therapeutic target for the relief of pain.
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Neuroscience letters · Aug 2008
Preconditioning with NMDA protects against toxicity of 3-nitropropionic acid or glutamate in cultured cerebellar granule neurons.
A brief sub-lethal ischaemic stimulus has been reported to protect against subsequent ischaemic damage in vivo, and in vitro following periods of hypoxia or oxygen-glucose deprivation (OGD). Preconditioning against neurotoxic stimuli has been linked to N-methyl-d-aspartate (NMDA) receptors, since receptor blockade prevents the protection afforded by OGD, and low doses of NMDA treatment are capable of preconditioning. The current study demonstrated that NMDA preconditioning also protects against 3-nitropropionic acid (3-NPA), a generator of both excitotoxic and oxidative damage, in addition to glutamate. ⋯ Neuronal viability was assessed by use of a fluorescein diacetate assay. Protection was effective with 100 microM NMDA preconditioning for 6 h against 1-100 microM glutamate, and also against 1-500 microM 3-NPA. The study demonstrates that NMDA preconditioning can be beneficial against excitotoxic treatments, even when these are potentially complicated by associated oxidative damage and metabolic compromise, as is the case for 3-NPA.