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)

We previously reported that food deprivation significantly decreased arginine-vasopressin (AVP) mRNA levels in the supraoptic (SON) and paraventricular (PVN) nuclei of the hypothalamus and also greatly stimulated the pituitary-adrenocortical system in rats. In this study, we deprived adrenalectomized rats with subcutaneously implanted low-dose corticosterone pellets (ADX + B) of food for 3 days to investigate the involvement of corticosteroid feedback regulation in the food deprivation-induced decrease in AVP mRNA in both the SON and the PVN. The plasma corticosterone levels in these animals were maintained at low levels constantly over 24 h. The ACTH concentration in the morning plasma was markedly increased in the food-deprived ADX + B rats as compared to the fed ADX + B rats. Food deprivation significantly decreased the corticotropin-releasing hormone (CRH) content in the median eminence and increased the CRH and AVP content in the neurointermediate lobe of the pituitary. Semiquantitative in situ hybridization histochemistry revealed that AVP mRNA levels were decreased in the SON but, inversely, increased in magnocellular as well as parvocellular subdivisions of the PVN following food deprivation. These results suggest that: (1) AVP mRNA responds differently to food deprivation between the SON and the PVN; (2) the glucocorticoid feedback can exert on AVP mRNA in the PVN but not in the SON in the food-deprived rats; and (3) food deprivation affects the neurohypophysial levels of CRH and AVP.
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PMID:The magnocellular arginine-vasopressin mRNA responds differently to food deprivation between the supraoptic and paraventricular nuclei of the hypothalamus in adrenalectomized rats with low corticosterone replacement. 150 43

The brain contains two types of adrenal steroid receptors, which play a role in mediating adrenal steroid effects on neuropeptide and other types of gene expression in discrete brain regions. Because the paraventricular nuclei of the hypothalamus (PVN) have adrenal steroid-sensitive neuropeptide systems, they provide a bench-mark to assess the doses of receptor agonists that may act selectively via Type I and Type II receptors. In the present study, in situ hybridization histochemistry was used to examine the effects of adrenalectomy (ADX) and Type I and Type II receptor agonists on arginine vasopressin (AVP) mRNA and corticotropin-releasing hormone (CRH) mRNA in rat brain. In agreement with previous reports, adrenal steroid regulation of AVP and CRH mRNA was found to be mediated primarily through the Type II receptor. Furthermore, adrenalectomy significantly increased AVP mRNA in the parvocellular region of the hypothalamic paraventricular nucleus (PVN), and systemic administration of the specific Type II agonist, RU28362 (10 micrograms/microliters/h), as well as corticosterone (CORT) pellets of 50 and 300 mg, prevented this increase. CRH mRNA was not significantly increased after ADX, but was markedly decreased in the PVN of rats receiving either RU28362 or a 300 mg pellet of CORT. Aldosterone, a specific Type I agonist, did not significantly affect either AVP or CRH mRNA levels when administered at 10 micrograms/h. Moreover, in the magnocellular regions of the PVN and SON AVP mRNA did not vary as a function of steroid manipulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of adrenalectomy and type I or type II glucocorticoid receptor activation on AVP and CRH mRNA in the rat hypothalamus. 785 39

Corticotropin releasing hormone (CRH), a major regulator of pituitary ACTH secretion, also acts as a neurotransmitter in the brain. To determine whether CRH is involved in the regulation of hypothalamic function during stress, CRH receptor binding and CRH receptor mRNA levels were studied in the hypothalamus of rats subjected to different stress paradigms: immobilization, a physical-psychological model; water deprivation and 2% saline intake, osmotic models; and i.p. hypertonic saline injection, a combined physical-psychological and osmotic model. In agreement with the distribution of CRH receptor binding in the brain, in situ hybridization studies using 35S-labeled cRNA probes revealed low levels of CRH receptor mRNA in the anterior hypothalamic area, which were unaffected after acute or chronic exposure to any of the stress paradigms used. Under basal conditions, there was no CRH binding or CRH receptor mRNA in the supraoptic (SON) or paraventricular (PVN) nuclei. However, 2 h after the initiation of acute immobilization, CRH receptor mRNA hybridization became evident in the parvicellular division of the PVN, with levels substantially increasing from 2 to 4 h, decreasing at 8 h and disappearing by 24 h. Identical hybridization patterns of CRH receptor mRNA were found in the parvicellular PVN after repeated immobilization; levels were similar to those after 2 h single stress following immobilization at 8-hourly intervals for 24 h (3 times), and very low, but clearly detectable 24 h after 8 or 14 days daily immobilization for 2 h. On the other hand, water deprivation for 24 or 60 h and intake of 2% NaCl for 12 days induced expression of CRH receptor mRNA in the SON and magnocellular PVN, but not in the parvicellular pars of the PVN.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Stress-specific regulation of corticotropin releasing hormone receptor expression in the paraventricular and supraoptic nuclei of the hypothalamus in the rat. 789 72

Previously, we showed that during salt-loading in mice there was an acute rise in plasma ACTH levels after 2 days followed by a transient decrease after 4 and 9 days. Pro-opiomelanocortin (POMC) mRNA levels in the anterior pituitary increased after 2 days and returned to normal thereafter. In this study, changes in hypothalamic CRH and AVP mRNA levels during salt-loading were investigated using quantitative in situ hybridization histochemistry. CRH mRNA was expressed only in the paraventricular nucleus (PVN), while AVP mRNA was expressed in both the supraoptic (SON) and paraventricular nuclei. CRH mRNA levels were unchanged after 2 days salt-loading, but declined to 77% of control levels after 9 days. AVP mRNA levels rose to 260% and 634% of control levels in the SON, and to 352% and 522% of control levels in the PVN, after 2 and 9 days salt-loading, respectively. These data suggest a major role of AVP in the acute stimulation of ACTH secretion and POMC mRNA levels seen after 2 days salt-loading. Desensitization of AVP receptors at the corticotroph level and a centrally mediated inhibition of CRH release may account for the decrease of ACTH secretion and POMC mRNA levels in the anterior pituitary with prolonged salt-loading.
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PMID:The effect of salt-loading on corticotropin releasing hormone and arginine vasopressin mRNA levels in the mouse hypothalamus: a quantitative in situ hybridization analysis. 824 54

Lewis (LEW/N) and Fisher (F344/N) rats are histocompatible inbred strains characterized respectively by susceptibility and resistance to inflammatory disease. LEW/N rats have deficient corticotropin-releasing hormone (CRH), ACTH and corticosterone responses to inflammation, and increased circulating and hypothalamic concentrations of arginine vasopressin (AVP). CRH is produced locally at inflammatory sites, where it acts as a proinflammatory agent, while AVP has been reported to exert immunopotentiating effects in vivo and in vitro. In order to further investigate the mechanism of increased AVP secretion in LEW/N rats, we measured AVP and CRH mRNA in several hypothalamic nuclei in LEW/N and F344/N rats, using in situ hybridization histochemistry. LEW/N rats had increased AVP mRNA concentrations in the supraoptic (SON) and paraventricular (PVN), but not in the suprachiasmatic (SCN) nuclei. CRH mRNA, on the other hand, was decreased in the PVN of LEW/N rats. To examine the potential role of AVP and CRH in the exaggerated inflammatory responses of LEW/N rats, we pretreated young female Lewis and Fischer rats with AVP- and/or CRH-neutralizing rabbit antisera and elicited subsequently an inflammatory response by a nuchal subcutaneous injection of carrageenin. We demonstrated that both antisera decreased significantly the leukocyte concentration in the inflammatory exudate in LEW/N rats, but found no synergistic or addictive effects between them. We conclude that previously observed differences in hypothalamic AVP and CRH contents between LEW/N and F344/N rats correspond to differences in the steady state mRNA levels of the two neuropeptides and that both AVP and CRH participate in the excessive inflammatory response of Lewis rats as locally active proinflammatory agents.
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PMID:Increased arginine vasopressin secretion may participate in the enhanced susceptibility of Lewis rats to inflammatory disease. 826 43

This study, the first using the pig, examined expression of mRNAs for vasopressin (VP), oxytocin (OT), preproenkephalin (PENK) and pro-opiomelanocortin (POMC) in the forebrain, and of POMC and prolactin in the pituitary. High basal expression of VP and OT mRNAs was present in the paraventricular (PVN) and supraoptic (SON) nuclei. In the PVN, VP was found in magnocellular regions whereas OT was also seen in the parvocellular portion; the distribution of VP and OT mRNAs in the SON was as reported in other species. The suprachiasmatic nucleus contained VP mRNA but only OT message was present in the dorsomedial SON, a structure peculiar to swine. Gene expression for PENK occurred in the caudate putamen (CPu), for POMC in the mediobasal hypothalamus (MBH) and for prolactin and POMC in the hypophysis. Following restraint, VP message increased in the magnocellular PVN, as did PENK in the CPu and POMC in the MBH.
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PMID:Vasopressin and oxytocin gene expression in the porcine forebrain under basal conditions and following acute stress. 941 19

Centrally administered histamine (HA) stimulates the secretion of the pro-opiomelanocortin-derived peptides ACTH and beta-endorphin as well as prolactin. The effect of HA on secretion of these adenohypophysial hormones is indirect and may involve activation of hypothalamic neurons containing corticotropin-releasing hormone (CRH), arginine-vasopressin (AVP) or oxytocin (OT). We studied the effect of activating central HA receptors by central infusion of HA, HA agonists or antagonists on expression of CRH, AVP and OT mRNA in the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei. Intracerebroventricular infusion of HA (270 nmol), the H1-receptor agonist 2-thiazolylethylamine or the H2-receptor agonist 4-methylhistamine increased the level of CRH mRNA in the PVN, and OT mRNA in the SON. In contrast, none of these compounds had any effect on expression of AVP mRNA in the PVN or SON. Administration of the H1-receptor antagonist mepyramine or the H2-receptor antagonist cimetidine had no effect on basal expression of CRH, AVP or OT mRNA in the PVN and/or SON except for a slight inhibitory effect of cimetidine on CRH mRNA expression in the PVN. Pretreatment with mepyramine or cimetidine before HA administration inhibited the HA-induced increase in OT mRNA levels but had no effect on the HA-induced increase in CRH mRNA levels in the PVN. We conclude that HA stimulates hypothalamic CRH and OT neurons by increasing mRNA levels, and this effect seems to be mediated via activation of both HA H1 and H2 receptors.
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PMID:Neuronal histamine and expression of corticotropin-releasing hormone, vasopressin and oxytocin in the hypothalamus: relative importance of H1 and H2 receptors. 972 83

While the present understanding of pituitary-adrenal function predicts attenuation of responses to a repeated stressor, experimental observations often show occurrence of potentiation rather than inhibition. The role of the CNS in this phenomenon was investigated in rats sustaining either a single (S-HEM) or a double episode (R-HEM) of hemorrhage. For S-HEM, blood was withdrawn over 3min and retransfused at 10min; for R-HEM, the stimulus was repeated at 90 min. S-HEM elicited 26- and 9-fold increases in circulating adrenocorticotropin (ACTH) and corticosterone, respectively. After R-HEM the plasma ACTH response was potentiated by 82%. Sixty min after S-HEM, Fos-like immunoreactivity (Fos-IR) was increased in medullary (solitary nucleus, NTS and ventrolateral medulla, VLM), pontine (locus coeruleus, LC and parabrachial nucleus, PBN), limbic (central amygdala, CNA and bed nucleus, BNST), and hypothalamic (supraoptic nucleus, SON and paraventricular nucleus, PVN) regions activated by hemodynamic stimuli. However after R-HEM, the Fos-IR response was significantly potentiated only in the VLM and PVN, while only a moderate increase was evident in the NTS. In other brain regions (LC, PBN, CNA, BNST, HPC and SON), Fos-IR either did not change or the increases were less than those observed after S-HEM. It is suggested that this plasticity in the pattern of neuronal activation following repetition of a stimulus may account for the maintenance of pituitary-adrenal secretory responses and its potentiation after R-HEM.
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PMID:Patterns of Fos-Immunoreactivity in the CNS Induced by Repeated Hemorrhage in Conscious Rats: Correlations with Pituitary-Adrenal Axis Activity. 978 63

Development of the neuroendocrine hypothalamus is characterized by a precise series of morphogenetic milestones culminating in terminal differentiation of neurosecretory cell lineages. The homeobox-containing gene Orthopedia (Otp) is expressed in neurons giving rise to the paraventricular (PVN), supraoptic (SON), anterior periventricular (aPV), and arcuate (ARN) nuclei throughout their development. Homozygous Otp(-/-) mice die soon after birth and display progressive impairment of crucial neuroendocrine developmental events such as reduced cell proliferation, abnormal cell migration, and failure in terminal differentiation of the parvocellular and magnocellular neurons of the aPV, PVN, SON, and ARN. Moreover, our data provide evidence that Otp and Sim1, a bHLH-PAS transcription factor that directs terminal differentiation of the PVN, SON, and aPV, act in parallel and are both required to maintain Brn2 expression which, in turn, is required for neuronal cell lineages secreting oxytocin (OT), arginine vasopressin (AVP), and corticotropin-releasing hormone (CRH).
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PMID:Progressive impairment of developing neuroendocrine cell lineages in the hypothalamus of mice lacking the Orthopedia gene. 1055 7

The presence of corticotropin-releasing hormone (CRH) receptors type-1 (CRHR-1) and type-2 (CRHR-2alpha) in the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei, and the effects of i.c.v. injection of CRH and urocortin on arginine vasopressin (AVP) and oxytocin release, have suggested that CRH ligands have a role in osmoregulation. In this study, double labelling in situ hybridization using 35S-labelled CRHR-1 or CRHR-2alpha and digoxigenin-labelled AVP, oxytocin or CRH riboprobes was employed to examine the localization of CRHR-1 or CRHR-2alpha mRNA in the SON and PVN of control and osmotically stimulated rats. Rats received an i.p. hypertonic saline (1.5 M) injection or isotonic saline injection (controls), or 2% NaCl intake (salt loading) or tap water (controls) for 12 days. While CRHR-1 mRNA was undetectable in the SON and PVN in control rats, its expression was increased markedly at 4 h after i.p. hypertonic saline injection or after 12 days salt loading. Of the cells labelled with digoxigenin-AVP, 53% in the SON and 90% in the PVN coexpressed CRHR-1 mRNA after i.p. hypertonic saline injection. In oxytocinergic neurones, 73% in the SON and 91% in the PVN showed CRHR-1 autoradiographic grains higher than background levels after i.p. hypertonic saline injection. In addition, i.p. hypertonic saline induced CRHR-1 mRNA expression in digoxigenin-CRH stained cells in the parvocellular PVN. CRHR-2alpha transcripts were present in both the SON and PVN under basal conditions, and salt loading, but not acute i.p. hypertonic saline injection, further stimulated this expression. Double labelling in situ hybridization showed colocalization of CRHR-2alpha mRNA with AVP and oxytocin mRNA in the SON. These studies support a role for CRH and urocortin regulating the hypothalamo-neurohypophyseal system, and suggest a direct action of the peptides in the magnocellular neurones.
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PMID:Vasopressin and oxytocin neurones of hypothalamic supraoptic and paraventricular nuclei co-express mRNA for Type-1 and Type-2 corticotropin-releasing hormone receptors. 1097 8


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