Pain
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Comparative Study
Oxycodone and morphine have distinctly different pharmacological profiles: radioligand binding and behavioural studies in two rat models of neuropathic pain.
Previously, we reported that oxycodone is a putative kappa-opioid agonist based on studies where intracerebroventricular (i.c.v.) pre-treatment of rats with the kappa-selective opioid antagonist, nor-binaltorphimine (nor-BNI), abolished i.c.v. oxycodone but not morphine antinociception, whereas pretreatment with i.c.v. naloxonazine (mu-selective antagonist) produced the opposite effects. In the present study, we used behavioural experiments in rat models of mechanical and biochemical nerve injury together with radioligand binding to further examine the pharmacology of oxycodone. Following chronic constriction injury (CCI) of the sciatic nerve in rats, the antinociceptive effects of intrathecal (i.t.) oxycodone, but not i.t. morphine, were abolished by nor-BNI. ⋯ In depleted brain membranes, the kappa(2b)-ligand, leu-enkephalin, prevented oxycodone's displacement of high-affinity [(3)H]bremazocine binding, suggesting the notion that oxycodone is a kappa(2b)-opioid ligand. Collectively, the present findings provide further support for the notion that oxycodone and morphine produce antinociception through distinctly different opioid receptor populations. Oxycodone appears to act as a kappa(2b)-opioid agonist with a relatively low affinity for mu-opioid receptors.
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Editorial Comment Review Comparative Study
How different is oxycodone from morphine?
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Comparative Study
Revelation of a personal placebo response: its effects on mood, attitudes and future placebo responding.
While ethics of placebo use has been debated since discovery of the phenomena, there has yet to be a study that examines the aftereffect of individuals learning of a personal placebo response on their future ability to experience a placebo response. In the first study, eleven participants diagnosed with irritable bowel syndrome in a placebo study were interviewed individually about their personal placebo response. We found no changes in attitudes about the likelihood of using medical and non-medical treatments for pain, likelihood of participating in future studies or likeability and trust of experimenters. ⋯ Using a heat thermode, we discovered that there were no differences in future pain responding between participants who were told that they experienced a placebo response versus those who were not. In addition, similar to the first study, we found no detrimental effects of the placebo information variables measured. These studies suggest the placebo response persists even after revelation of a personal placebo response and placebo use does not appear to cause adverse effects on mood and other attitude variables assessed.
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Comparative Study
Peripheral and central components of habituation of heat pain perception and evoked potentials in humans.
For the neurophysiological examination of nociceptive pathways, contact-heat evoked potentials (contact-heat EPs) are elicited by repetitive brief noxious heat stimuli. Suppression of heat responses in primary nociceptive neurons during repetitive stimulation has been shown in animal models in vivo and in vitro. We now investigated whether heat pain and contact-heat EPs in humans display equivalent signs of habituation. ⋯ As a consequence, both measures were significantly reduced (p<0.005) leading to a rightward shift of the stimulus-response function by 5 degrees C. In conclusion, human heat pain perception and contact-heat EPs display signs of rapid habituation when stimulation is restricted to a fixed location and thus, reflect fatigue of peripheral nociceptive neurons. Habituation within the central nervous system is slower and less pronounced.
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Flashbacks in posttraumatic stress disorder (PTSD) are commonly experienced as visual, auditory, olfactory or tactile re-livings of a previously experienced traumatic event. We present the case report of one survivor of the July 7th 2005 London underground bombings who was diagnosed with PTSD and who experienced painful flashbacks. ⋯ The case provides further evidence that somatosensory re-experiencing of pain memories is possible. Findings are discussed with regards to memory for pain.