Pain
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The aims of this study were to replicate and extend previous observations on the relationship between enmeshment of the self and pain and measures of adjustment [Morley et al., Possible selves in chronic pain: self-pain enmeshment, adjustment and acceptance, Pain 2005;115:84-94], and to test the hypothesis that individual variation in motivational preferences interacts with enmeshment. 82 chronic pain patients completed standardized self-report measures of depression, anxiety, acceptance and the possible selves interview which generated measures of their hoped-for (own and other perspectives) and feared-for selves. They made judgments about the conditionality of each self on the continuing presence of pain as a measure of self-pain enmeshment. A series of hierarchical regression analyses, that adjusted for demographics, pain characteristics and disability, confirmed the relationship between self enmeshment and depression and acceptance. When anxiety was considered, there was no main effect for any of the self aspects but there were specific interactions between the hoped-for (own) and (other) selves and two motivational preferences--autonomy and sociotropy.
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Since neuropathic pain is resistant to conventional analgesics such as opiates and non-steroidal anti-inflammatory drugs, the development of new types of drugs for its treatment has been awaited. Several key molecules associated with nociception have been suggested as potential targets for new analgesics. Glial cell line-derived neurotrophic factor (GDNF) has a variety of functions affecting the survival and development of specified neural cell populations, mediated via transmission of intracellular signals through binding to its high-affinity receptor, GFR*1, and subsequent activation of a tyrosine receptor kinase, RET, neural cell adhesion molecule (NCAM), or other signaling molecules. ⋯ Reduction of NCAM expression by NCAM antisense oligodeoxynucleotide administration to CCI rats abolished the analgesic effect of GDNF without affecting RET signaling activation. An NCAM mimetic peptide, C3d, partially reduced the chronic pain induced by CCI. These findings suggest that NCAM signaling plays a critical role in the analgesic effect of GDNF and that development of new drugs activating GDNF-NCAM signaling may represent a new strategy for the relief of intractable pain.
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The aim of the present study is to get an insight into the pain report of children over two sequential dental visits. Furthermore, it was studied whether age, previous dental experience, level of dental anxiety and injection site were of influence on the self-reported pain of children during the first and second treatment session. One hundred and forty-seven children (4-11 years old) were included in the study. ⋯ For the older children, the children having previous dental experience gave the highest pain ratings on the first treatment session. Furthermore, for both young and older children the amount of pain reported for the second injection was best predicted by the amount of pain reported for the first injection, whereby higher scores the first time predict higher scores the second time. In conclusion, the memory of previous experience with dentistry and earlier treatment sessions seems of great influence on the behaviour and the experience of children during subsequent treatment sessions.
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Windup is a progressive, frequency-dependent increase in the excitability of trigeminal and spinal dorsal horn wide dynamic range (WDR) nociceptive neurons to repetitive stimulation of primary afferent nociceptive C-fibers. Superficial dorsal horn neurokinin 1 receptor (NK1R)-expressing neurons were recently shown to regulate sensitization of WDR nociceptive neurons through activation of a defined spino-bulbo-spinal loop. However, the windup of WDR nociceptive neurons was not regulated through this loop. ⋯ Second, we anatomically identified in the MDH lamina III a subpopulation of NK1R-expressing local interneurons that relay nociceptive information from the MDH to downstream Sp5O neurons. Third, using microinjections of NK1R antagonists during in vivo electrophysiological recordings from Sp5O WDR neurons, we showed that WDR neuron windup depends on activation of NK1Rs located in the MDH laminae I-III. We conclude that, in contrast to central sensitization that is controlled by a spino-bulbo-spinal loop, Sp5O WDR neuron windup is regulated through a local circuit activated by MDH lamina III NK1Rs.
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This study investigated the effect of haeme oxygenase-1 (HO-1) in nociception induced by formalin injection in the mice hind paw. Intraperitoneal (i.p.) administration of cobalt protoporphyrin (CoPP, an HO-1 inducer, 5mg/kg) 24h before the test, inhibited the nociceptive response during the second phase, but not during the first phase of the formalin test. The effect of CoPP was prevented by treatment with tin protoporphyrin (SnPP, an inhibitor of HO-1 activity) administered either by i.p. (25mg/kg, 30 min before the test) or intraplantar (400 nmol/paw, 5 min before the test) routes. ⋯ In conclusion, Nrf2-mediated HO-1 expression induced an antinociceptive effect at peripheral sites. These results suggest that HO-1 modulates the inflammatory pain pathways. Hence, the development of drugs that could raise peripheral HO-1 could be relevant in inflammatory pain treatment.