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

Proliferation of corticotrophs following adrenalectomy (ADX) was studied by a combination of bromodeoxyuridine (BrdU)-labeling and immunohistochemistry. Rats were adrenalectomized, allowed to survive for 1, 3, 7, and 14 days and given 100 mg/kg body wt BrdU 3 h before sacrifice. BrdU and adrenocorticotropic hormone (ACTH) were detected in the same sections of the anterior pituitary using double-labeling immunohistochemistry. BrdU-labeled cells in the pituitary showed a tendency to increase until 1 week after ADX and slightly decreased at 2 weeks. Corticotrophs were increased to about 1.5 times of the control level 1-2 weeks after ADX. The number of cells double-labeled with both BrdU and ACTH increased markedly after ADX, suggesting active mitosis of existing corticotrophs. On the other hand, the ratios of these double-stained cells to all BrdU-labeled cells and to all corticotrophs were 5-7% and 0.9-1.3%, respectively, even after ADX, suggesting that the majority of corticotrophs which were increased after ADX were recruited from some other type of immature cells. The extent to which the two mechanisms are involved in hyperplasia of corticotrophs after ADX remains to be elucidated.
 ...
PMID:Proliferation of pituitary corticotrophs following adrenalectomy as revealed by immunohistochemistry combined with bromodeoxyuridine-labeling. 763 51

Recent investigations revealed that adrenalectomized (ADX) rat pups exhibit deficits in behavioral inhibition. Furthermore, administration of exogenous corticosterone (CORT) restores behavioral inhibition in ADX pups. Although these studies suggest that CORT has an important role in the development of behavioral inhibition, the relative behavioral effects of elevated pituitary hormone secretion induced by ADX are not known. Therefore, experiments were conducted to assess the potential behavioral effects of elevated adrenocorticotropin (ACTH) secretion induced by ADX and to further evaluate the contribution of endogenous CORT to the development of behavioral inhibition. In Experiment 1., we verified that 10-day-old ADX rats exhibit high levels of plasma ACTH throughout the preweaning period associated with the development of behavioral inhibition. In Experiment 2, 10-day-old pups were hypophysectomized (HYPOX) and ADX and were compared behaviorally to sham-operated controls on day 14. When tested in the presence of an anesthetized unfamiliar adult male rat, HYPOX + ADX pups exhibited low levels of freezing accompanied by ultrasonic vocalizations. These pups also had reduced concentrations of plasma ACTH and CORT. In Experiment 3, 10-day-old pups were HYPOX and tested for behavioral inhibition on day 14. In comparison to sham-operated controls, HYPOX rats exhibited significantly lower levels of freezing and had reduced plasma concentrations of ACTH and CORT. Results demonstrate clearly that deficits in freezing occur even in the presence of low plasma ACTH concentrations. Therefore, elevated secretion of pituitary hormones is not a major factor that contributes to the ADX-induced deficits in behavioral inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Relative contributions of pituitary-adrenal hormones to the ontogeny of behavioral inhibition in the rat. 777 8

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)
 ...
PMID:Effects of adrenalectomy and type I or type II glucocorticoid receptor activation on AVP and CRH mRNA in the rat hypothalamus. 785 39

This study was designed to examine adrenocortical function in old (30 months) and young (6 months) male Brown Norway rats. The following observations were made. First, stress induced a higher pituitary adrenocorticotropic hormone (ACTH) response in the aged male Brown Norway rats than in young rats, while peak circulating corticosterone (CORT) levels were not different. Moreover, this type of "repeated" stress involving subcutaneous injection and blood sampling at various time points by pinching the tail vein, evoked a prolonged ACTH and CORT response in the aged animal. Second, exogenous ACTH1-24 administered to dexamethasone-pretreated Brown Norway rats, used as an in vivo challenge test for adrenocortical function, resulted in a delayed CORT response in the aged rats. The termination of the CORT response to ACTH, however, was not different between young and old rats. Third, ACTH1-24 stimulation of adrenocortical cells in vitro showed a tendency to a reduced CORT output, when these cells were obtained from old animals. Fourth, adrenalectomy (ADX) differentially affected pituitary ACTH release at both ages. The initial post-ADX ACTH surge was more pronounced in the aged animals. Beyond 4 days post-ADX the old Brown Norway rats did not show the pronounced afternoon peak in circulating ACTH as was observed in the young animals. This study demonstrates that during the aging process a deficiency in adrenocortical function develops in the male Brown Norway rat. This deficiency involves a less efficient stress-induced activation of adrenocortical output of CORT having enhanced pituitary ACTH release as one of the consequences.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Adrenocortical hyporesponsiveness and glucocorticoid feedback resistance in old male brown Norway rats. 787 84

The ACTH response to CRF and the role of glucocorticoids on the pituitary-adrenal responsiveness to acute stressors after a period of chronic stress were assessed in Sprague-Dawley rats. After chronic immobilization (IMO) an enhanced ACTH response to CRF administration was observed. In another experiment, control and chronic IMO rats were adrenalectomized (ADX) or sham-adrenalectomized (SHAM) and 2 days later killed in resting conditions or after having been subjected to acute IMO or tail-shock for 30 min. Chronic IMO increased basal corticosterone but not adrenocorticotropin (ACTH) levels in SHAM rats. As expected, ADX increased ACTH levels in all conditions. In response to the novel acute stressor (shock), ACTH levels were drastically dependent on the presence of corticosterone: thus, whereas in SHAM rats chronic IMO reduced the ACTH response to shock, in ADX rats a clear enhancement of the ACTH response to shock was observed in chronic IMO rats. In order to demonstrate that, in our experimental conditions, chronic stress also induces down-regulation of glucocorticoid receptors in the hippocampus, an additional experiment was done: rats subjected chronically to IMO or administered 5 mg corticosterone (B) were adrenalectomized and killed 20 h later under basal conditions. Both chronic IMO and chronic B administration decreased glucocorticoid type II binding in the hippocampus. From these results, it is concluded that chronic IMO induces facilitation of the ACTH response to novel acute stressors which is uncovered after corticosterone removal.
 ...
PMID:Direct evidence for chronic stress-induced facilitation of the adrenocorticotropin response to a novel acute stressor. 809 Feb 76

Possible interactions between alcohol (EtOH) and interleukins (ILs) were studied in intact and adrenalectomized (ADX) rats. In intact animals, administration of 0.3 or 0.65 g EtOH/kg 30 min to 4 hr earlier did not cause measurable changes in plasma adrenocorticotropic hormone (ACTH) levels measured immediately before acute intravenous injection of IL-1 beta or endotoxin [lipopolysaccharide (LPS)], and did not interfere with the ability of either treatments to increase ACTH secretion. Administration of 1.5 g EtOH/kg, on the other hand, resulted in elevated plasma ACTH and corticosterone 30 min later, and significantly decreased the magnitude of the ACTH response to IL-1 beta in both intact and ADX rats. When administered 4 hr before the cytokine, however, 1.5 g EtOH/kg did not alter the responsiveness of the hypothalamic-pituitary-adrenal (HPA) axis to IL-1 beta. Studies of the reverse paradigm were conducted in rats injected with LPS, a means of increasing endogenous IL-1 levels. Intraperitoneal administration of alcohol 4 hr later resulted in measurably blunted ACTH release by intact rats, but not ADX animals. We conclude that when prior alcohol administration does not result in elevated ACTH levels at the time of IL-1 injection, no alteration in the HPA axis' response to the cytokine is observed. As we have shown in other experiments that circulating levels of corticosterone were temporarily increased by all doses of alcohol used in the present study, these results suggest that steroid feedback did not play a major role in modulating the ability of IL-1 beta to activate the HPA axis.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Acute interactions between cytokines and alcohol on ACTH and corticosterone secretion in the rat. 827 79

Adjuvant-induced arthritis (AA) in specific strains of rats is an immunologically mediated inflammatory disease which is also characterised by activation of the endocrine system. To further investigate the effects of AA on processing of the pro-opiomelanocortin (POMC) precursor in rat immune tissues, we utilised radioimmunoassays for adrenocorticotrophin (ACTH), beta-endorphin and alpha-melanocyte-stimulating hormone (alpha-MSH) to measure these peptides in the spleen and thymus. 14 days following adjuvant injection, spleen levels of ACTH were elevated in the AA group (4.47 +/- 1.04 ng/g tissue, n = 9) compared to controls (2.42 +/- 0.4 ng/g) and exacerbation of the disease by removal of circulating glucocorticoids through bilateral adrenalectomy (ADX) resulted in further elevation of spleen ACTH (5.11 +/- 1.22 ng/g). beta-Endorphin levels in both the AA (10.60 +/- 1.61 ng/g) and AA/ADX (13.37 +/- 2.36 ng/g) groups were higher than controls (5.57 +/- 0.65 ng/g). Conversely, alpha-MSH spleen levels were decreased in the AA (2.89 +/- 0.22 ng/g) and AA/ADX (2.22 +/- 0.33 ng/g) groups compared to controls (4.62 +/- 0.45 ng/g) and were also decreased following adrenalectomy. In the thymus, ACTH levels were elevated in the AA group (8.95 +/- 1.41 ng/g) compared to controls (5.79 +/- 0.63 ng/g), and the same pattern was evident for thymic alpha-MSH (0.64 +/- 0.08 ng/g in AA animals compared to control levels of 0.35 +/- 0.03 ng/g). Following G50 gel filtration, ACTH and beta-endorphin immunoreactivities (ir) were present in both spleen and thymus as two peaks, one which eluted near the void volume and one which eluted in a lower molecular mass position than the standards.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effects of a chronic inflammatory stress on levels of pro-opiomelanocortin-derived peptides in the rat spleen and thymus. 829 57

Following three 24 hourly serial injections of 4-aminopyrazolo[3,4-d]pyrimidine (4-APP) to rats, the levels of plasma corticotropin (ACTH) and of adrenal HMG-CoA reductase, the cholesterol side chain cleavage system, 3 beta-hydroxysteroid dehydrogenase, 21-hydroxylase, and adrenodoxin increased after an initial lag of 17 h. In contrast the mRNA level of 11 beta-hydroxylase was differently regulated since it was elevated after 17 and 24 h and decreased thereafter to basal values. These increases appear to be related to ACTH secretion since they were blocked by the coadministration of dexamethasone (Dex) and 4-APP. Also 3 h after the administration of Dex to 4-APP treated rats rapid decreases in plasma corticosterone and ACTH levels were accompanied by decreases in mRNA levels of HMG-CoA reductase and low density lipoprotein receptor, two components involved in the synthesis and transport of cholesterol. The mRNA level of the electron donor adrenodoxin was also decreased, suggesting that this component participates in the short term regulation of corticosterone synthesis in the rat adrenal. The adrenal response was more readily observed with components involved in the steps preceding cholesterol biosynthesis than in those subsequent to cholesterol in the corticosteroid pathway. However, the effects of 4-APP on the latter pathway were well documented with mRNA analysis performed by Northern blot, a more sensitive technique than the Western blot used for protein quantification. The entire metabolism of the corticosterone biosynthetic pathway was thus affected in rats treated with 4-APP. Taken collectively these results indicate that under acute lipoprotein depletion rat adrenals developed a compensatory mechanism enabling them to synthesize and utilize cholesterol for corticosteroid synthesis.
 ...
PMID:Effects of dexamethasone on the levels of adrenal steroidogenic enzyme mRNA in rats treated with 4-aminopyrazolopyrimidine. 839 95

The present study investigates the role of corticotropin-releasing hormone (CRH) neurons in stress regulation by a comparison of stress induced Fos-immunoreactivity and CRH-immunoreactivity in the hypothalamic paraventricular nucleus (PVH) of APO-SUS (apomorphine-susceptible), APO-UNSUS (apomorphine-unsusceptible), normal Wistar and adrenalectomized Wistar (ADX) rats. The first two types represent a good model to study the role of the PVH in stress regulation, since they show different stress responses and a differential synaptic organization of the PVH. After placement on an open field for 15 min all rats showed an increase in the number of Fos-immunoreactive nuclei compared to control handling. Interestingly, open field stress, but not control handling, induces significantly fewer Fos-immunoreactive nuclei in the PVH of APO-SUS rats (1255 +/- 49) compared to APO-UNSUS rats (1832 +/- 201). Experiments with ADX rats revealed that 93% of the CRH-immunoreactive neurons contained a Fos-immunoreactive nucleus, which suggests that the differential Fos-expression in APO-SUS and APO-UNSUS rats represents a differential activation of the CRH neurons. This hypothesis is discussed in relation to reported differences in stress responses, stress-induced ACTH levels and synaptic organization of the PVH.
 ...
PMID:The hypothalamic paraventricular nucleus in two types of Wistar rats with different stress responses. II. Differential Fos-expression. 852 6

Immuno- and hybridization histochemical methods were used to examine a possible role for adrenocorticotropic hormone (ACTH) in regulating the expression of corticotropin-releasing peptides in rat hypothalamus. Densitometric assessments of relative levels of mRNAs encoding corticotropin releasing factor (CRF), arginine vasopressin (AVP) and oxytocin (OT) in the parvocellular division of the paraventricular nucleus (PVH) were carried out in intact, adrenalectomized (ADX) and hypophysectomized (HYPOX) animals. Both surgeries resulted in comparable increases in relative levels of CRF and AVP transcripts in the parvocellular PVH; no effects on OT mRNA in this compartment were evident. In a second experiment, ACTH or saline vehicle were administered systemically via osmotic minipump for seven days to rats submitted to both HYPOX and ADX surgeries. Lower replacement doses of ACTH reduced the number of detectable AVP-immunoreactive (AVP-ir) cells in the parvocellular PVH to 53% of that seen in vehicle-treated HYPOX/ADX controls; the number of CRF-IR cells was not significantly affected. Higher doses of ACTH resulted in counts of AVP- and CRF-IR neurons that were reduced to 32% and 70%, respectively, of control values. Staining patterns for the two peptides in the external lamina of the median eminence generally followed the cell count data. Neither densitometric nor combined immunohistochemical (for CRF-ir) and hybridization histochemical (for AVP mRNA) assays revealed any marked effect of ACTH on AVP mRNA expression in the parvocellular PVH of HYPOX/ADX rats. The results indicate that ACTH is capable of inhibiting corticotropin-releasing peptide, but not mRNA, expression in hypophysiotropic neurons. The mechanisms underlying these effects remain to be fully clarified.
 ...
PMID:Evidence for short-loop feedback effects of ACTH on CRF and vasopressin expression in parvocellular neurosecretory neurons. 854 50


<< Previous 1 2 3 4 5 6 7 8 9 Next >>