Neuroreport
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Randomized Controlled Trial Clinical Trial
Systemic adenosine attenuates touch evoked allodynia induced by mustard oil in humans.
The effect of adenosine on tactile allodynia (secondary hyperalgesia) was studied in 6 healthy volunteers, using a double-blind, placebo controlled, cross-over design. Tactile allodynia was induced by topical application of mustard oil on the skin of the volar aspect of the forearm. ⋯ The threshold for eliciting allodynia with von Frey filaments was not influenced by adenosine. The study shows that adenosine can reduce the area of mustard oil induced tactile allodynia.
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Levels of nerve growth factor (NGF) in rat hindpaw skin, measured with a sensitive two-site enzyme-linked immunosorbent assay, show two peaks during normal development. The first (57 +/- 5 pg mg-1) occurs at embryonic days (E) 18-20 and coincides with the arrival of axon terminals into the hindpaw skin. ⋯ Skin wounding at birth produces a marked increase in NGF levels (149 +/- 25 pg mg-1) which declines after 4 days. This large increase is not observed if wounding is performed at older ages and may underlie the sensory hyperinnervation that accompanies neonatal wounds.
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The effects of the metabotropic glutamate receptor (mGluR) agonist ACPD ((1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid) on single neurones and on the network underlying locomotion in the lamprey have been analysed. ACPD induces a depolarization in lamprey spinal cord neurones, which is insensitive to tetrodotoxin (TTX) and ionotropic glutamate receptor antagonists, but is reversibly blocked by the mGluR antagonist MCPG ((+)-alpha-methyl-4-carboxyphenylglycine). The ACPD-induced depolarization persists in a calcium-free solution or when the calcium channel blocker cadmium is added to the solution. At the network level ACPD causes an increased burst frequency during fictive locomotion by increasing the excitability level of network neurones.
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We examined the effects of intrathecal oxytocin over a wide dose range (10 ng to 10 micrograms) on the spinal nociceptive flexor reflex in decerebrate, spinalized, unanaesthetized rats. Oxytocin facilitated the flexor reflex at all doses. ⋯ No reflex depression was observed with intrathecal oxytocin at any dose. It is suggested that activation of spinal oxytocin receptors excites the spinal cord and therefore intrathecal oxytocin is unlikely to be an analgesic agent.
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The aim of the present study was to investigate whether clonidine and morphine interact positively to produce analgesia against the low intensity tonic pain represented by the formalin model in rats. Sub-threshold doses of morphine (0.5 mg kg-1) and clonidine (0.025 mg kg-1) were found to elicit marked antinociceptive effects when co-administered intraperitoneally, 15 min prior to formalin challenge. ⋯ Clonidine and morphine thus exhibit a supra-additive effect against low intensity pain with negligible potential for induction of tolerance. This finding may be relevant for the long term control of chronic pain in certain clinical conditions.