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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous research has suggested that a short-term (6 week) high-intensity and a subsequent long-term (1 year) low-intensity dynamic training programme in 8 patients with rheumatoid arthritis (RA) increased circulating levels of beta-endorphin (beta-EP) during the high-intensity training and of corticotropin-releasing factor (CRF) and beta-lipotropin (beta-LPH) levels during the low-intensity training, without an increase of pain experience. The present follow-up study of the patients, using the data obtained after an additional 1-year period of no standardized training as reference values, indicated that CRF levels decreased significantly (P less than 0.01) in relation to those obtained 1 year earlier. For beta-LPH and beta-EP, no corresponding decreases were noted. No significant difference concerning experience of pain over time was found. High-performance liquid chromatography demonstrated a complex elution pattern with low basal concentration of beta-LPH, which increased after 60 min of training.
Pain 1992 Apr
PMID:Dynamic training and circulating neuropeptides in rheumatoid arthritis: a two-year follow-up study. 159 83

By means of double immunolabeling procedures it has been possible to demonstrate glucocorticoid receptor (GR) immunoreactivity (IR) in large numbers of various peptidergic neurons of the brain including neurons containing gastrointestinal peptides, opioid peptides, and peptides with a hypothalamic hormone function. For each peptide system, however, marked heterogeneities exist among brain regions. Thus, in the neocortex and the hippocampal formation most of the brain peptide neurons lack GR IR, while the same types of peptide neurons in the arcuate and paraventricular nucleus [e.g. neuropeptide Y (NPY), somatostatin (SRIF) and the cholecystokinin (CCK) neurons] possess strong GR IR. Furthermore, in the arcuate, parvocellular part of the paraventricular nuclei and the central amygdaloid nucleus practically all the peptidergic neurons are strongly GR IR, while in the lateral hypothalamus, mainly the neurotensin (NT) and galanin (GAL) IR neurons are GR IR. These marked differences among areas probably reflect functional differences dependent upon their participation in stress regulated circuits. All the paraventricular NT, corticotropin-releasing factor (CRF), growth hormone-releasing factor (GRF), thyrotropin-releasing hormone (TRH) and SRIF IR neurons appear to contain GR IR, while the luteinizing hormone-releasing hormone (LHRH) IR neurons lack GR IR, underlying the importance of glucocorticoids (GC) in controlling endocrine function. Finally, the GC may influence pain and mood control mainly via effects on enkephalin (ENK) neurons especially in the basal ganglia (mood) and on all beta-endorphin (beta-END) neurons of the arcuate nucleus, while most of the dynorphin neurons are not directly controlled by GC.
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PMID:Central peptidergic neurons as targets for glucocorticoid action. Evidence for the presence of glucocorticoid receptor immunoreactivity in various types of classes of peptidergic neurons. 168 65

The influence of prolonged pain upon hypothalamic opioid peptide release in vitro was examined in rats subjected to Freund's adjuvant (FA)-induced unilateral inflammation of the hindlimb. Basal release of enkephalin (ENK) but not beta-endorphin (END) or dynorphin (DYN) was increased 10 days following FA treatment. Superfusion of corticotropin-releasing factor (CRF; 10(-8) M) stimulated the release of opioid peptides in control hypothalami. CRF, however, failed to modify beta-END and DYN release in hypothalami of FA-treated rats, whereas ENK release was markedly reduced. In contrast, KCl-stimulated opioid peptide release did not differ between FA and control hypothalami. These data demonstrate that prolonged inflammatory pain alters the responsiveness of hypothalamic opioid systems to CRF. It is suggested that this effect is mediated at the level of the CRF neuron or its receptor.
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PMID:Prolonged inflammatory pain modifies corticotropin-releasing factor-induced opioid peptide release in the hypothalamus. 168 11

The effect of dexamethasone on exercise-induced adrenocorticotropin (ACTH) secretion and dental analgesia was studied in healthy human subjects. Different levels of exercise (100-200 W) were produced by a cycle ergometer. Dental pain thresholds were tested with a constant current stimulator. Dental pain thresholds were elevated with increasing work loads, and the elevation was still significant 30 min after the end of the exercise. Dexamethasone produced a significant reversal of exercise-induced pain threshold elevations concomitantly with the suppression of exercise-induced ACTH release. The results suggest that the corticotropin releasing factor-ACTH axis is involved in the exercise-induced analgesia.
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PMID:Dexamethasone attenuates exercise-induced dental analgesia in man. 216 84

The study aimed at evaluating the effects of a dynamic training program on circulating levels of corticotropin-releasing factor (CRF), beta-lipotropin (beta-LPH), and beta-endorphin (beta-EP) in 8 patients (5 females and 3 males, aged 39-65 years) with classical/definite rheumatoid arthritis (RA). Blood samples were collected immediately before, in the middle of, and after a 6-week high-intensity training period as well as after a subsequent 1-year period of low-intensity training. In addition, baseline data were obtained 3 weeks before the start of the training program. Use of multivariate analyses of variance, and of analyses of variance of contrast variables, indicated a short-term effect of the high-intensity training program for beta-EP with increased levels (P less than 0.05) between the 3rd and the 6th weeks, no significant differences being obtained for CRF or beta-LPH here. Corresponding analyses with regard to the combined high and low-intensity training program revealed CRF (P less than 0.01), and beta-LPH (P less than 0.01) levels to increase over time, no long-term effect being found for beta-EP. Despite the intensity of the dynamic training program, no change was found in pain experience as measured on a visual analogue scale.
Pain 1990 Jan
PMID:Dynamic training and circulating levels of corticotropin-releasing factor, beta-lipotropin and beta-endorphin in rheumatoid arthritis. 233 14

Corticotropin-releasing hormone and endogenous opioid peptide systems are both activated during stress. An elevation of the pain threshold also occurs under conditions of stress. In the present study the effects of CRH antinociception were examined. Rats were treated with CRH either centrally (i.c.v.) or peripherally (intracardially; i.c.) and their tail-flick latencies were measured. Central application of CRH (0-30 micrograms) was without effect on the analgesic test, while after peripheral application (0-32 micrograms) CRH produced a dose-dependent increase in tail-flick latencies. In a subsequent experiment we examined the possible involvement of endogenous opioids in the peripheral CRH-induced antinociceptive effects. To this end, two approaches were used: animals were either acutely treated with the opioid antagonist naloxone (3 or 6 mg/kg), or they were rendered tolerant to morphine, and then tested with CRH. In both cases, CRH effects on the tail-flick latencies were not modified. Our findings suggest that: (a) CRH may modulate pain sensitivity during stress; (b) opioids do not mediate this effect; and (c) brain CRH receptors are probably not involved in these processes.
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PMID:Peripheral but not intracerebroventricular corticotropin-releasing hormone (CRH) produces antinociception which is not opioid mediated. 260 16

Using antiserums generated against the neuropeptides corticotropin-releasing factor (CRF), beta-endorphin, and adrenocorticotropin, we have immunocytochemically mapped the organization of these hormones throughout the brain. The distribution of CRF perikarya is widespread throughout the forebrain, brain stem, and spinal cord. The central opiomelanocortin system is represented by two separate pools of neuronal perikarya: the hypothalamic arcuate pool, and the medullary (nucleus tractus solitarius) pool. From these groups fibers distribute widely throughout forebrain and brain stem. A conspicuous codistribution pattern exists between the CRF perikarya and opiomelanocortin fibers. Analysis of these systems within the brain stem and spinal cord reveals innervation and distribution patterns within regions containing catecholamine systems, areas associated with regulation of sympathetic and parasympathetic outflow, cardiovascular and respiratory homeostatic centers, and regions associated with stress, autonomic homeostasis, and pain modulation. By virtue of these extensive brain-stem distributions, it is suggested that an anatomical substrate exists for participation of these peptide systems in the integration of certain autonomic, visceral, and homeostatic mechanisms.
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PMID:Anatomy of the corticotropin-releasing factor and opiomelanocortin systems of the brain. 298 28

The dose-response relationship of neonatal (days 1-7) administration of beta-endorphin (BE) and corticotropin-releasing factor (CRF) on body weight, eye opening, response to thermal pain, and concentrations of plasma and adrenal corticosterone were measured in developing rat pups. At the highest dose (50 micrograms/pup), neonatal CRF reduced body weight, while 10 and 50 micrograms/pup accelerated eye opening. In addition, a reduction in concentration of plasma and adrenal corticosterone was correlated with the dose of neonatal CRF, whereas adrenal weights were not altered. BE produced none of these effects, but 1, 10 and 50 micrograms/pup on days 1-7 significantly reduced baseline latencies in a novel water-bath tail-flick test on day 9. These same animals showed reduced numbers of brain opiate receptors on day 14. The results indicate that peptide administration during the sensitive neonatal period can alter the development of physiological processes that will later be influenced by the peptide.
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PMID:Neonatal peptides affect developing rats: beta-endorphin alters nociception and opiate receptors, corticotropin-releasing factor alters corticosterone. 301 83

The analgesic activity of corticotropin releasing factor (CRF) was determined in a clinical model and in the rat hot plate test. Patients administered CRF reported significantly less postoperative pain than patients pretreated with placebo. In rats, injection of CRF resulted in a significant analgesia which was comparable in both intensity and duration to a 300 times greater molar dose of morphine. These findings suggest that endogenous CRF may play a physiologic role in modulating pain when released under conditions of stress.
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PMID:Corticotropin-releasing factor (CRF) produces analgesia in humans and rats. 331 18

The nucleus paragigantocellularis lateralis (PGi) in the rostral ventral medulla is implicated in several functions including cardiovascular control, respiration, pain and analgesia. More recent studies implicate this region in alertness and attention as well, by virtue of its prominent projections to the nucleus locus coeruleus (LC). To investigate information that is integrated in the PGi, we used tract tracing to examine brain and spinal projections to this region. Afferents to PGi were found to be functionally diverse and topographically organized. Projections to the retrofacial PGi are primarily autonomic in nature. A wider range of inputs were found to target the rostral (juxtafacial) aspect of the PGi, including brain nuclei involved in the processing of somatosensory and auditory stimuli, as well as autonomic areas. Efferent projections to the LC were also examined in detail. Neuropharmacology experiments revealed that the PGi provides a potent excitatory amino acid input to the LC and an inhibitory input acting at alpha 2 receptors on LC neurons. PGi neurons projecting to the LC stained for markers of adrenaline, enkephalin, GABA and corticotropin releasing factor. Finally, some PGi neurons collateralize to innervate both the LC and the spinal cord. These results suggest that the LC may function in parallel to peripheral autonomic systems providing a cognitive complement to sympathetic function, and that the PGi may integrate a wide range of inputs to facilitate adaptive responses to urgent environmental events.
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PMID:Integration in the ventral medulla and coordination of sympathetic, pain and arousal functions. 773 66


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