Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution of corticotropin-releasing hormone-immunoreactive (CRH-IR) neurons and fibers was observed in golden hamsters. CRH-IR neurons and fibers were observed within the hypothalamus, thalamus, amygdala, cortex, midbrain, and hindbrain. The largest numbers of CRH-IR neurons were seen within the magno- and parvocellular divisions of the paraventricular nucleus of the hypothalamus and within the septum, bed nucleus of the stria terminalis, preoptic area continuum. The highest density of immunoreactive fibers was observed in the external zone of the median eminence. In addition, many immunoreactive fibers were observed within the bed nucleus of the stria terminalis and the preoptic area. The distribution obtained in hamsters was compared with previously reported distributions from rats, and both were generally similar.
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PMID:Distribution of corticotropin-releasing hormone immunoreactivity in golden hamster brain. 142 65

The effects of noxious and non-noxious mechanical stimulation of various segmental skin areas (face, forelimb and forepaw, abdomen, hindlimb and hindpaw) on the secretion of immunoreactive corticotropin-releasing hormone (iCRH) from the hypothalamus into hypophysial portal blood was examined in artificially ventilated rats under halothane anesthesia. Secretion of iCRH was calculated from the iCRH concentration in hypophysial portal plasma and the plasma flow rate. Noxious mechanical stimulation of the skin was delivered by pinching using surgical clamps, while non-noxious mechanical stimulation was provided by brushing with tooth brushes. Pinching of the bilateral forepaws or hindpaws and brushing of the bilateral hindlimbs for 20 min increased hypothalamic iCRH secretion. In contrast, pinching of the face or abdomen and brushing of the face, forelimbs, or abdomen for 20 min did not significantly influence it. These results indicate that cutaneous mechanical sensory stimulation contributes to the reflex regulation of CRH secretion from the hypothalamus into hypophysial portal blood, and also that this effect is highly dependent on the site of stimulation.
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PMID:Hypothalamic corticotropin-releasing hormone (CRH) secretion into hypophysial portal blood is regulated by cutaneous sensory stimulation in anesthetized rats. 143 8

The regulation of human corticotropin-releasing hormone (hCRH) gene promoter activity by inducers of cAMP was investigated by transient transfection with a construct containing the hCRH gene promoter fused to the chloramphenicol acetyltransferase gene. Expression of hCRH-chloramphenicol acetyltransferase was strongly enhanced by forskolin in the neuroblastoma SK-N-MC and choriocarcinoma JAR cell lines. Overexpression of the catalytic subunit of protein kinase A dispensed the need for forskolin, and cotransfection of cAMP-responsive element-binding protein cDNAs enhanced forskolin-dependent expression of the hCRH promoter. Progressive 5'-end deletions of the hCRH promoter delineated a cAMP- responsive region between -226 and -164 base pairs. This fragment contained the sequence TGACGTCA at -221 base pairs, consistent with the consensus motif for a CRE. A homologous oligonucleotide responded to cAMP when cloned in either orientation in front of the thymidine kinase promoter. However, the level of constitutive and inductive cAMP expression was dependent on the cell line and on intrinsic properties of the promoter. Mutation of the wild type CRH-CRE sequence into an AP-1 site (TGAGTCA) completely abolished stimulation by cAMP. In contrast, coexpression of the catalytic subunit of protein kinase A dispensed the need for stimulation with forskolin, which showed that the CRH-CRE oligonucleotide served as a functional equivalent of the native CRE element.
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PMID:Identification and characterization of a 3',5'-cyclic adenosine monophosphate-responsive element in the human corticotropin-releasing hormone gene promoter. 148 Jan 79

The effects of emotional stress (ES) corresponding to conditioned fear on colonic motility and its antagonism by [deamino-Pen1, Val4, D-Arg8]vasopressin, a vasopressin antagonist, were investigated by electromyography in conscious fasted rats fitted with chronically implanted electrodes. A 117% increase (19.6 +/- 2.1 vs. 9.0 +/- 0.9 cycles/10 min during the control period) in the frequency of colonic spike bursts was observed when rats were placed for 30 min in a box in which they had previously received electric foot shocks. Intracerebroventricular (icv) administration of corticotropin-releasing hormone (CRH; 0.5 micrograms/kg) mimicked the effects of ES and increased the spike burst frequency of the colon by 88.6% from 5 to 15 min after its administration. At doses between 5 and 20 micrograms/kg the antagonist [deamino-Pen1, Val4, D-Arg8]vasopressin significantly reduced or abolished the effects of ES and CRH administration on colonic motility. Injected icv at doses of 2.5 and 5 ng/kg [Arg8]vasopressin dose dependently increased the frequency of colonic spike bursts. These effects were not reproduced by similar or higher (50 ng/kg) doses given intraperitoneally, and the effects were abolished after previous administration of vasopressin at a dose of 20 micrograms/kg. It is concluded that the effects of ES on colonic motility in rats previously shown to be linked to the central nervous system (CNS) release of CRH are in turn mediated through the central release of vasopressin.
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PMID:CNS vasopressin mediates emotional stress and CRH-induced colonic motor alterations in rats. 155 Feb 33

A 14-year-old girl has been suffering from an isolated adrenocorticotropin hormone (ACTH) deficiency with secondary glucocorticoid deficiency and common variable immunodeficiency since the age of 6.6 years. Human corticotropin releasing hormone administration did not increase ACTH and cortisol levels, strongly suggesting a pituitary deficiency. Despite the profound humoral defect, severe infections have never developed and the antibody response to herpes viruses was intact. We speculate that the association between two rare disorders, simultaneously diagnosed 2 months after measles, is not coincidental but caused by close interactions between neuro-endocrine and immune systems.
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PMID:Isolated adrenocorticotropic hormone deficiency associated with common variable immunodeficiency. 164 68

Plasma concentrations of corticotropin releasing hormone (CRH) and the serum concentrations of luteinizing hormone (LH), follicle stimulating hormone (FSH), testosterone, adrenocorticotropic hormone (ACTH) and cortisol were measured in seven physically active males after acute exercise on a treadmill using the Bruce protocol. Measurements were made in the basal pre-exercise state, immediately after exercise, and at 30-min intervals for 3 h after exercise. Serum LH concentrations declined following exercise reaching nadir values between 60 and 180 min after exercise (90 min post exercise in the group). The nadir values in individual volunteers were significantly lower than both the baseline and post-exercise levels. This fall in serum LH concentration appeared to follow a slight but significant elevation of the plasma concentration of CRH which reached peak levels when measured immediately post exercise. Plasma ACTH concentrations paralleled the rise in CRH, but fell to undetectable levels of below 13.8 nmol.l-1 (less than 5 ng.l-1) 60 min after exercise. Plasma cortisol concentrations peaked approximately 30 min after the rise in ACTH, after which they gradually declined to baseline levels. Plasma testosterone concentrations paralleled the concentrations of LH. The data suggest that CRH, on the basis of its previously described gonadotropin-depressant property, may be the hormone involved in the exercise-mediated decline in serum LH. Alternatively, some as yet unidentified factor(s), may be involved in producing the altered concentrations of both LH and CRH.
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PMID:Corticotropin releasing hormone and gonadotropin secretion in physically active males after acute exercise. 164 5

Endothelin-3 (ET-3) is a member of the novel vasoconstrictive peptide family, identified in porcine central nervous system. Intravenous bolus injection of 1000 pmol/kg of ET-3 in freely moving rats caused significant increases in plasma ACTH and corticosterone levels, almost equivalent to those of 100 pmol/kg of rat corticotropin-releasing hormone (rCRH). The action of ET-3 was virtually abolished by pretreatment of CRH-antagonist, alpha-helical CRH. When ET-3 was added to cultured anterior pituitary cells, neither direct stimulation of ACTH release nor potentiation of rCRH action was noted. The results indicate that ET-3 may function as a neuropeptide and stimulation of the CRH-neurons, direct or inderect, is mainly responsible for activation of ACTH and corticosterone release.
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PMID:Endothelin-3 stimulates the hypothalamic-pituitary-adrenal axis. 164 64

CRH (corticotropin-releasing hormone) is a hypothalamic polypeptide that stimulates ACTH secretion by the anterior pituitary and, subsequently, cortisol secretion by the adrenal cortex. CRH test administration is indicated in the differential diagnosis of Cushing syndrome and in the assessment of corticotropic function in different pituitary conditions. Both human CRH (hCRH) and ovine CRH (oCRH) can be used by i.v. injection. Intrinsic ACTH-releasing activities of the two molecular forms are similar. Nevertheless, and contrary to hCRH, oCRH does not interact with the human CRH specific binding protein (CRH-BP) and the use of this ovine form could be useful in testing pituitary function while avoiding possible changes in peptide activity due to protein binding. The present study was conducted in 3 distinct groups of human volunteers to evaluated the ACTH and cortisol responses to i.v. oCRH (1 micrograms per kg body weight) at noon (oCRH test). 24 healthy, nonobese subjects, not under medication, participated in the study. The first group consisted of 8 young men, the second of 8 women of childbearing age and the third of 8 menopausal women. Tolerance to the oCRH test was excellent in all 3 groups. A significant increase in plasma ACTH and cortisol was observed in all the subjects, with peak occurrence for ACTH between 15 and 60 minutes after oCRH and between 20 and 120 minutes for cortisol. The responses were not sex-related among the young subjects, but the menopausal women displayed a higher cortisol increase than the other 2 groups.
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PMID:[Test with ovine corticotropin-releasing hormone (oCRH): clinical application and reference values in the young adult and the postmenopausal women]. 164 82

Using autoradiography combined with immunocytochemistry, we demonstrated that the target cells of CRH in the human pituitary were proopiomelanocortin cells. Scatchard analysis of [125I]Tyr0-oCRH saturation binding revealed the presence of one class of saturable, high affinity sites on pituitary tissue homogenate. The equilibrium dissociation constant (Kd) for [125I]Tyr0-oCRH ranged from 1.1-1.6 nM, and the receptor density was between 200-350 fmol/mg protein. Fixation of cryostat sections with 4% paraformaldehyde before tracer incubation improved both tissue preservation and localization of the CRH receptor at the cellular level. Additional postfixation with 1% glutaraldehyde inhibited tracer diffusion during subsequent immunocytochemistry and autoradiography. [125I]Tyr0-oCRH was found in cytoplasmic inclusions or at the cell periphery of ACTH/beta-endorphin cells in the anterior pituitary. Single cells of the posterior pituitary were also CRH receptor positive. Cells staining for PRL or GH were CRH receptor negative. We conclude that CRH binds only to high affinity receptors on ACTH/beta-endorphin cells in the human pituitary.
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PMID:Receptors for corticotropin-releasing hormone in human pituitary: binding characteristics and autoradiographic localization to immunocytochemically defined proopiomelanocortin cells. 164 37

Corticosteroid type I and II receptors mediate the negative feedback effects of these hormones at various central nervous system sites involved in the regulation of the hypothalamic-pituitary-adrenal (HPA) axis. To examine the effects of chronic treatment with dexamethasone (DEX), a type 2 receptor agonist, on the regulation of this axis, male Sprague-Dawley rats weighing 200-250 g were given daily injections of DEX for 1,2,3, and 4 weeks or were treated with a subcutaneously implanted DEX-releasing minipump for one week. At the end of treatment, the animals were weighed and brains and truncal blood were collected. Daily intermittent DEX treatment reduced the body weight of the rats in a time-dependent fashion, but had little or no effect on their wet brain weight. Plasma ACTH and corticosterone, measured by RIA, were fully suppressed after one week of intermittent treatment and did not show any further reduction in rats treated for longer periods. In these animals, the content of immunoreactive corticotropin-releasing hormone (iCRH), arginine vasopressin (AVP), ACTH and beta-endorphin (beta-EP) in the hypothalamus, hippocampus, cerebral cortex and cerebellum and pituitary ACTH content did not show any difference compared to vehicle-treated rats. In contrast, continuous DEX treatment increased iCRH content in the cortex, reduced AVP content in the cerebellum, increased ACTH content in the hippocampus, decreased ACTH and beta-EP content in the hypothalamus, and reduced pituitary ACTH content. Hypothalami explanted from rats treated with DEX for one week released lower basal amounts of iCRH in vitro and did not respond to a maximally stimulatory concentration of serotonin (5-HT), a known CRH secretagogue. Continuous DEX administration suppressed also potassium chloride-induced iCRH release. Interestingly, hypothalami explanted from rats receiving daily injection of vehicle, but not from unhandled, untreated controls, did not respond to 5-HT with an increase of iCRH release in vitro. In conclusion, prolonged and continuous, but not intermittent, administration of DEX had a strong effect on brain neuropeptide content. Both regimens of DEX reduced the hypothalamic iCRH responsiveness to stimuli in vitro. Chronic handling also decreased the responsiveness of the hypothalamus to a stimulatory neurotransmitter and may confound the interpretation of data pertinent to inhibitory mechanisms.
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PMID:Hypothalamic and suprahypothalamic effects of prolonged treatment with dexamethasone in the rat. 165 Aug 4


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