Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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

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 intensity of neuronal uptake of 3H- or 14C-labeled GABA, glycine, noradrenaline, choline and glucocorticoid receptor binding were investigated in different structures of the rabbit CNS by simulating chronic pain syndrome. Data obtained allow to suggest pathogenetically justified therapy including the complexes of phenybute + atropine and relanium + atropine. The contents of Leu-Enkephaline, cortisol, insuline and insuline/cortizole ratio were studied in the blood serum of the patients with neurological manifestations of lumbar osteochondrosis and a long case history of the pain treated by the above mentioned complexes. The proposed therapeutical approach allowed to achieve pronounced antistress effect and regression of the pain syndrome due to stimulation of the CNS endogenic antinociceptive structures. It was shown that stress-produced hormones and opioids ratio in the blood serum may serveas indirect criteria of the functional activity of the endogenic antinociceptive structures before and after the treatment.
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PMID:[Pathogenetic basis for the use of GABA-ergic preparations in combination with atropine during chronic pain syndrome in patients with neurologic manifestations of lumbar osteochondrosis]. 1080 84

The effects of dexamethasone pretreatment on clonidine-induced antinociception and locomotor hypoactivity were investigated in mice. In the hot-plate and the tail-flick tests, dexamethasone administered intraperitoneally at a dose of 1 mg kg(-1), 30 or 60 min before clonidine, reduced clonidine antinociception in both tests and reduced clonidine-induced locomotor hypoactivity in the activity cage. When administered 15 min before clonidine, dexamethasone had no effect on clonidine antinociception. A higher dexamethasone dose (10 mg kg(-1)) induced the same effects observed at a dose of 1 mg kg(-1) in the hot-plate and the tail-flick tests, but the former dose had a stronger effect on locomotor hypoactivity. Dexamethasone (10 ng/mouse) administered intracerebroventricularly 30 min before clonidine was also able to reduce both clonidine-induced antinociception and locomotor hypoactivity. The protein synthesis inhibitor, cycloheximide, administered intraperitoneally at the dose of 10 mg kg(-1), 2 h before clonidine, was able to prevent dexamethasone effects on clonidine-induced antinociception. The glucocorticoid receptor antagonist RU-38486, administered intracerebroventricularly at the dose of 1 ng/mouse, was also able to block dexamethasone effects on clonidine-induced antinociception and locomotor hypoactivity, whereas both cycloheximide and RU-38486 per se did not influence pain sensitivity or locomotor activity. These results suggest that the dexamethasone effects on clonidine-induced antinociception and locomotor hypoactivity depend on the stimulating effects that dexamethasone exert, on the protein synthesis via the glucocorticoid receptor in the brain.
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PMID:Clonidine-induced antinociception and locomotor hypoactivity are reduced by dexamethasone in mice. 1129 50

Estrogens exhibit complex but beneficial effects on brain structure, function and behavior. Soy-derived dietary phytoestrogens protect against hormone-dependent and age-related diseases, due to their estrogen-like hormonal actions. However, the effects of phytoestrogens on brain and behavior are relatively unknown. This study examined the influence of exposing male Long-Evans rats (lifelong) to either a phytoestrogen-rich (Phyto-600) or a phytoestrogen-free (Phyto-free) diet on body weights, behavioral pain thresholds, the hypothalamic-pituitary-adrenal (HPA) hormonal stress response, hippocampal glucocorticoid receptor and brain neural cell adhesion molecules (NCAM) and synaptophysin levels using standard behavioral and biochemical techniques. Body weights were significantly decreased in Phyto-600 fed animals compared to Phyto-free values. There were no significant changes in behavioral pain thresholds, circulating corticosterone concentrations (after acute immobilization stress) or NCAM and synaptophysin levels in various brain regions by the diet treatments. However, Phyto-600 fed males displayed significantly higher plasma adrenocorticotrophin (ACTH) (post-stress) and hippocampal glucocorticoid receptor levels vs. Phyto-free values. These data suggest that (1) body weights are significantly reduced by soy-derived phytoestrogens, (2) behavioral pain thresholds (via heat stimuli) are not influenced by dietary phytoestrogens, but (3) these estrogenic molecules in the hippocampus enhance glucocorticoid receptor abundance and alter the negative feedback of stress hormones towards a female-like pattern of higher ACTH release after activation of the HPA stress axis. This study is the first to show that lifelong consumption of dietary phytoestrogens alters the HPA stress response in male rats.
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PMID:Stress (hypothalamic-pituitary-adrenal axis) and pain response in male rats exposed lifelong to high vs. low phytoestrogen diets. 1272 19

Central administration of 15 ng interleukin (IL)-1beta in the rat significantly enhanced conditioned fear memory assessed by a passive avoidance task, when retested at 24 and 48 h post-training. Pain threshold was unaffected by 15 ng IL-1beta administration. IL-1beta treatment also increased serum corticosterone. This increase in serum corticosterone was further enhanced in rats given both IL-1beta and footshock. Furthermore, the glucocorticoid receptor antagonist mifepristone blocked IL-1beta-induced elevation in corticosterone and also attenuated the enhanced conditioned fear memory. Central administration of IL-1beta significantly increased prostaglandin E2 and decreased the anti-inflammatory cytokine IL-10 release from whole blood cultures; therefore this treatment appears to be effective in inducing an inflammatory response in both the periphery and the brain. The present study confirms that IL-1beta can enhance conditioned fear memory, an effect which is correlated with changes in glucocorticoid function. This facilitation of defensive behaviour could reflect adaptive responses which may enhance survival during sickness.
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PMID:Interleukin 1 beta enhances conditioned fear memory in rats: possible involvement of glucocorticoids. 1462 8

Dexamethasone is commonly used to limit the severity of chronic lung disease in premature infants with severe respiratory distress syndrome. Recent literature has demonstrated an association between dexamethasone exposure in critically ill premature neonates and later development of cerebral palsy. However, the majority of children exposed to dexamethasone in the neonatal period do not develop cerebral palsy or global developmental delay, and other more subtle effects of early life glucocorticoid exposure may go unnoticed. Presently, little is known regarding possible effects of early dexamethasone exposure on development of neuropeptide systems that are sensitive to glucocorticoid modulation. One such system is the pain-related opioid system that interacts with the stress-related limbic-hypothalamic pituitary adrenal (LHPA) axis. In the present study, a neonatal rat model was used to expose newborn rats to dexamethasone. Using a within-litter design, on postnatal days P3 through P6, pups were either handled, or they received a daily intramuscular injection of saline or dexamethasone. Adult animals were sacrificed on day of life P120, their brains were removed and quick-frozen. Using in situ hybridization histochemistry, mRNA expression of the opioid receptor-like (ORL1) receptor was measured in the paraventricular nucleus of the hypothalamus (PVN) and the hippocampal formation. In dexamethasone-treated adult male rats, ORL1 mRNA expression was increased in the PVN and dentate gyrus, but decreased in area CA1, when compared to handled and vehicle controls. These results suggest that prolonged glucocorticoid receptor (GR) occupation in the neonatal period leads to permanent alterations in ORL1 expression in the LHPA stress axis of the adult rat.
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PMID:Dexamethasone exposure during the neonatal period alters ORL1 mRNA expression in the hypothalamic paraventricular nucleus and hippocampus of the adult rat. 1464 7

Perinatally, the first encounter between the maturing receptor and its target hormone results in hormonal imprinting, which adjusts the binding capacity of the receptor for life. In the presence of an excess of the target hormone or foreign molecules than can be bound by the receptor, faulty imprinting carries life-long consequences. In cytogenic organs, imprinting could also be provoked in other periods of life (late imprinting). Imprinting also durably influences the production of the imprinter and related hormones. In the present study, single beta-endorphin doses was given to three-week old female rats at 3 microg/animal, and the serotonin in five brain regions (frontal cortex, striatum, hippocampus, hypothalamus and brain stem) and uterine estrogen receptor content were determined, thymic glucocorticoid receptor binding capacity was measured, and sexual behavior was tested at five months of age. Brain serotonin levels highly significantly decreased, while sexual activity (Meyerson index and lordosis quotient) increased. At the same time, uterine estrogen receptor affinity decreased. There was no change in receptor binding capacity in the thymus. We will go on to discuss interrelations between the results. The experiments demonstrate that a non-perinatal treatment with a molecule acting at receptor level (late imprinting) can also lastingly influence various indexes in non-cytogenic organs. The results call attention to the possible long-lasting influence of an endorphin surge (caused, for example, by pain) on brain serotonin content and sexual behavior.
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PMID:Endorphin excess at weaning durably influences sexual activity, uterine estrogen receptor's binding capacity and brain serotonin level of female rats. 1498 5

Fractionation of an anti-inflammatory extract from Cayaponia tayuya roots yielded two active compounds, identified as 23,24-dihydrocucurbitacin B (1) and cucurbitacin R (2). Both were evaluated for their anti-inflammatory activity on several experimental models of pain and inflammation. In addition, their cytotoxicity and effects on leukotriene B4 (LTB4) formation were evaluated in rat polymorphonuclear leukocytes. Both compounds showed activity in the following models: carrageenan-induced mouse paw oedema (1, 4 mg/kg p.o., 46% inhibition at 3 h), phospholipase A2-induced mouse paw oedema (2, 3 mg/kg i.p., 61% inhibition at 60 min), serotonin-induced mouse paw oedema (1 and 2, 0.5 mg/kg s.c., 73% and 79% inhibition, respectively), 12- O-tetradecanoylphorbol 13-acetate (TPA)-induced acute ear oedema (2, 36% inhibition at 4 mg/kg p.o., and 87% inhibition at 0.1 mg/ear topically). The compounds were also active against the inflammation induced by repeated application of TPA on mouse ears, affecting both the oedema itself (1 and 2 at 0.1 mg/ear, 44% and 56% inhibition, respectively) as well as cell infiltration (68% and 69%, respectively). The activity of both compounds against oedema induced by serotonin was not modified by the glucocorticoid receptor antagonist mifepristone; however, the protein synthesis inhibitor cycloheximide abolished the anti-inflammatory response in both cases. Neither compound modified the production of LTB4 in rat polymorphonuclear leukocytes, nor did they exhibit analgesic properties at the dose assayed.
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PMID:Anti-inflammatory activity of two cucurbitacins isolated from Cayaponia tayuya roots. 1512 85

Injury to the spinal nerves of mice induces mechanical allodynia and thermal hyperalgesia. In the injured spinal cord, the expression of glucocorticoid receptor mRNA was increased, whereas it was decreased in N-type Ca(2+)-channel-deficient mice, in which neuropathic pain is eliminated. Intrathecal and intraperitoneal injection of the glucocorticoid receptor antagonist RU486 produced antinociceptive effects, whereas intracerebroventricular injection was without effect. The more selective antagonist dexamethasone 21-mesylate suppressed both mechanical allodynia and thermal hyperalgesia. These results suggest that spinal glucocorticoid receptors play an important role in neuropathic pain, and that controlling the activity of glucocorticoid receptors may be of great importance in the treatment of neuropathic pain.
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PMID:Effects of glucocorticoid receptor antagonists on allodynia and hyperalgesia in mouse model of neuropathic pain. 1625 2

Chronic pain can be considered a form of chronic stress, and chronic pain patients often have disturbances of the hypothalamic-pituitary-adrenal (HPA) axis, including abnormal cortisol levels. In addition, chronic pain patients have an increased incidence of depression and anxiety, stress-related disorders that are frequently accompanied by disturbances in the limbic system (e.g. hippocampus and amygdala) and the HPA axis. Despite the fact that the literature supports a strong link between chronic pain, stress disorders, and limbic dysfunction, the mechanisms underlying the effects of chronic pain on the HPA axis and limbic system are not understood. The current study employs a rodent neuropathic pain model (chronic constriction injury (CCI) of the sciatic nerve) to assess the long-term impact of chronic pain on the HPA axis and limbic system. Adult male rats received CCI or sham surgery; nociceptive behavioral testing confirmed CCI-induced neuropathic pain. Tests of HPA axis function at 13-23 days postsurgery demonstrated that CCI did not affect indices of basal or restraint stress-induced HPA axis activity. CCI increased the expression of corticotrophin releasing hormone mRNA in the central amygdala, and not the paraventricular nucleus of the hypothalamus or the bed nucleus of the stria terminalis. Moreover, glucocorticoid receptor mRNA expression in CCI rats was increased in the medial and central amygdala, unaffected in the paraventricular nucleus, and decreased in the hippocampus. These results suggest that increased nociceptive sensitivity during chronic pain is associated with alterations in the limbic system, but is dissociated from HPA axis activation.
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PMID:Limbic and HPA axis function in an animal model of chronic neuropathic pain. 1664 26


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