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)

In the light of evidence for endogenous opioid peptide involvement in the modulation of pituitary hormone release and in the body's overall response to stress, the aim of the present study was to determine the beta-endorphin-like immunoreactivity (beta-END-LI) in the blood plasma of ewes during different phases of the estrous cycle and in anestrous ewes subjected to acute or intermittent prolonged footshocks. The highest concentration of beta-END-LI was found in the blood plasma during the luteal phase and lowest one during the follicular stage at proestrus. Nearly equal concentrations of beta-END-LI were determined at estrus and metestrus; their values were over 10 times lower than those observed in the luteal phase. Acute stress caused transient increase of beta-END-LI in the blood plasma of anestrous ewes, with a peak after 15-30 min of footshock application and changes in the molar ratio of beta-LPH to beta-endorphin. No apparent increase in mean daily levels of beta-END-LI was noted in ewes subjected to prolonged footshocking; however, on the day after stimulation beta-END-LI concentration decreased below control values. These results indicate that: 1. secretion of beta-END-LI varies during different phases of the estrous cycle, 2. acute stress is a potent activator for beta-END-LI secretion, 3. no apparent increase of beta-END-LI in the blood plasma of ewes subjected to prolonged stress concomitant with accumulation of this material in pituitary (Polkowska and Przekop, 1988) supports the idea, that prolonged stress augments the synthesis of beta-END-LI but not its release.
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PMID:Changes in beta-endorphin-like-immunoreactivity in the blood plasma of ewes during estrous cycle and in anestrous ewes under stress condition. 224 20

The effect of immobilization stress on the expression of c-fos protein in the adrenal cortex of adult rats was investigated immunocytochemically. After immobilization stress lasting for longer than 30 min, an enhanced c-fos-like immunoreactivity was observed in the cortical cells of the zona fasciculata and zona reticulata. Compared to unstressed controls, an about 5-fold increase in the density of the immunoreactive cells in a unit of the cortical area was seen following a 1-h immobilization. The enhanced immunoreactivity lasted for at least 3 h after 1-h immobilization and it began to diminish 5 h after the stress. Furthermore, administration of dexamethasone 2 h prior to 1-h immobilization attenuated the stress-enhanced immunostaining for the c-fos-like protein. These results suggest that an acute stress may cause a dramatic and long-persisting induction of c-fos-like protein in the cortical cells of rat adrenals. The characteristic zonal distribution of the c-fos induction in rat adrenals as well as the effect of dexamethasone suggest involvement of the pituitary adrenocorticotropic hormone (ACTH) in the induction.
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PMID:Induction of c-fos-like protein in the rat adrenal cortex by acute stress--immunocytochemical evidence. 255 26

We have recently demonstrated that the pineal neurohormone melatonin can enhance immune reactivity in normal mice and counteract the effects of acute stress or corticosterone treatment on antibody production, thymus weight and anti-viral resistance. These remarkable immunopharmacologic effects of melatonin were abolished by naltrexone, suggesting an involvement of the endogenous opioid system. Here we compared the immunopharmacologic action of beta-endorphin, dynorphin 1-13, leu-enkephalin and metenkephalin with that of melatonin in restraint-stressed or prednisolone-treated mice and in normal nonstressed animals. We found that beta-endorphin and dynorphin 1-13 can mimic the immunoenhancing and antistress effect of melatonin. However, at variance with the pineal neurohormone, these opioids were effective in umprimed mcie, too. We found also that restraint stress or prednisolone treatment decreases the immunopharmacologic potency of beta-endorphin and augments that of dynorphin 1-13. In fact, at the doses used, beta-endorphin enhanced the antibody response in normal but not in stressed or prednisolone-treated mice, while dynorphin 1-13 was effective only in counteracting the effect of stress or prednisolone treatment. Most interestingly, all these effects proved to be dependent on the time of administration, i.e. showed a circadian rhythm in analogy with the effects of melatonin. Again, naltrexone abolished all the opioid effects, indicating that their action was exerted via opioid receptors. These findings have important scientific and practical implications.
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PMID:Beta-endorphin and dynorphin mimic the circadian immunoenhancing and anti-stress effects of melatonin. 257 Jul 59

Previous studies have indicated that acute stress in vivo or ovine corticotropin releasing hormone (oCRH) in vitro, releases both beta-lipotropin (beta-LPH) and beta-endorphin (beta-END) from the anterior lobe, with beta-END predominating over beta-LPH by 2:1. However, repeated stress shifts this ratio to proportionately more beta-LPH released with re-stress or oCRH in vitro. Alternative hypotheses were that the glucocorticoids released during stress altered the processing of proopiomelanocortin (POMC) or that the increased biosynthetic drive resulted in an inability of the processing enzymes to keep pace with biosynthesis. To distinguish between these alternatives, adrenalectomy studies were performed. Following removal of glucocorticoid negative feedback there is greatly increased secretion of beta-END-IR from anterior lobe corticotrophs with a subsequent increase in biosynthetic drive. Under these conditions of increased biosynthetic drive in the absence of steroids, the corticotroph secretes primarily beta-LPH, suggesting that increased biosynthetic drive alters the posttranslational processing rate of POMC.
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PMID:Adrenalectomy increases beta-lipotropin secretion over beta-endorphin secretion from anterior pituitary corticotrophs. 260 76

Hormones of the limbic-hypothalamic-pituitary-adrenocortical (LHPA) system are much involved in central nervous system regulation. The major LHPA neuropeptides, corticotropin-releasing hormone (CRH), vasopressin (AVP) and corticotropin (ACTH) do not only coordinate the neuroendocrine response to stress, but also induce behavioral adaptation. Transcription and post-translational processing of these neuropeptides is regulated by corticosteroids secreted from the adrenal cortex after stimulation by ACTH and other proopiomelanocortin derived peptides. These steroids play a key role as regulators of cell development, homeostatic maintenance and adaptation to environmental challenges. They execute vitally important actions through genomic effects resulting in altered gene expression and nongenomic effects leading to altered neuronal excitability. Since excessive secretory activity of this particular neuroendocrine system is part of an acute stress response or depressive symptom pattern, there is good reason to suspect that central actions of these steroids and peptides are involved in pathophysiology determining the clinical phenotype, drug response and relapse liability. This overview summarizes the clinical neuroendocrine investigations of the author and his collaborators, while they worked at the Department of Psychiatry in Mainz. The major conclusions from this work were: (1) aberrant hormonal responses to challenges with dexamethasone, ACTH or CRH are reflecting altered brain physiology in affective illness and related disorders; (2) hormones of the LHPA axis influence also nonendocrine behavioral systems such as sleep EEG; (3) physiologically significant interactions exist between LHPA hormones, the thyroid, growth hormone, gonadal and other neuroendocrine systems; (4) hormones of the LHPA axis constitute a bidirectional link between immunoregulation and brain activity; and (5) future psychiatric research topics such as molecular genetics of affective disorders, familial risk studies, drug response analysis and neurobiology of aging will benefit from extended knowledge of neural corticosteroid effects at a clinical, cellular, and molecular level.
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PMID:Psychiatric implications of altered limbic-hypothalamic-pituitary-adrenocortical activity. 267 May 76

Although cannabinoids exert strong effects on brain function, there have been no extensive analyses of the long-term effects of cannabinoids on mammalian brain structure. Consequently, we conducted quantitative light and electron microscopic studies on the brains of rats treated chronically with delta 9-tetrahydrocannabinol (THC) (5 X weekly for 8 months--approximately 30% of the life-span). In these studies, we found significant THC-induced changes in hippocampal structure: specifically, THC-treated animals exhibited decreased neuronal density and increased glial cell reactivity (i.e. an increase of cytoplasmic inclusions). In addition, we confirmed prior reports of THC-induced increases in adrenal-pituitary activity, since both adrenocorticotropic hormone (ACTH) and corticosterone were elevated substantially during an acute stress. However, the animals appeared to be only minimally affected behaviorally by the doses used (highest dose: 8 mg/kg) and no effects of THC were observed on several ultrastructural variables, including synaptic density. The observed hippocampal morphometric effects of chronic THC are similar to apparent glucocorticoid-dependent changes that previously have been found to develop in rat hippocampus during normal aging. Given that cannabinoids and steroids are similar in chemical structure in several respects, therefore, the present results seem to raise the possibility that chronic THC exposure may alter hippocampal anatomical structure by interactions with, or mimicry of, adrenal steroid activity.
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PMID:Quantitative changes in hippocampal structure following long-term exposure to delta 9-tetrahydrocannabinol: possible mediation by glucocorticoid systems. 283 17

Immunoreactive beta-endorphin (IR-BE) levels in the plasma, anterior pituitary (AP), the neurointermediate lobe of the pituitary (NIL), and the hypothalamus were determined in castrated female rats and castrated female rats treated with estradiol benzoate (estrogen), after exposure to acute (once for 45 min) or chronic (45 min each day for 15 consecutive days) immobilization stress. Acute and chronic stress increased plasma levels of IR-BE to the same extent in castrated female rats and castrated female rats treated with estrogen. In castrated female rats, acute stress produced an increase in the concentration of IR-BE in the AP, which was attenuated by the administration of estrogen. Although IR-BE in the NIL was not influenced by acute stress in castrated animals, exposure to acute stress resulted in an elevation in IR-BE levels in the NIL of rats given estrogen. Chronic stress did not affect the concentration of IR-BE in the AP of castrated females or castrated females treated with estrogen. Chronic stress did, however, increase the concentration of IR-BE in the NIL of castrated animals. This affect of stress on IR-BE levels in the NIL was potentiated by estrogen administration. IR-BE levels in the hypothalamus were reduced by estrogen and were not affected by acute or chronic stress, regardless of the gonadal steroid environment. As determined by column chromatography, administration of estrogen, as well as subjection to chronic stress, promoted the processing of the proopiomelanocortin precursor to form beta-lipotropin rather than beta-endorphin in the AP. By these methods, the only immunoreactivity detected in the NIL and the hypothalamus was beta-endorphin. These data indicate that IR-BE levels in the plasma, the AP, and the NIL of female rats are affected by immobilization stress and that estrogen modulates the effects of acute immobilization stress on IR-BE levels in the AP and the NIL and the effects of chronic immobilization stress on the levels of IR-BE in the NIL.
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PMID:Estrogen influences the effect of immobilization stress on immunoreactive beta-endorphin levels in the female rat pituitary. 296 43

Immunoreactive beta-endorphin (IR-BE) levels were determined in the anterior pituitary (AP), neurointermediate lobe of the pituitary (NIL) and the hypothalamus of castrated male rats and castrated male rats treated with testosterone proprionate (TP), subsequent to exposure to acute (once for 45 min) or chronic (45 min each day for 15 consecutive days) immobilization stress. Acute stress resulted in a reduction in the concentration of IR-BE in the AP of castrated male rats, which was potentiated by TP. The concentration of IR-BE in the NIL was elevated by acute stress in castrated male rats and was not affected by acute stress in castrated male rats administered TP. Exposure to chronic immobilization stress elevated the concentration of IR-BE in the AP of castrated animals and not animals treated with TP. The concentration of IR-BE in the NIL of castrated animals was not altered by chronic immobilization. Chronic stress did result in a significant rise in the level of IR-BE in the NIL of castrated male rats given TP. Hypothlamic IR-BE levels in castrated male rats were reduced by TP and were not influenced by acute or chronic stress. Chromatographic analysis indicated that acute and chronic stress promoted the accumulation of beta-lipotropin rather than beta-endorphin in the AP. This effect was attenuated by TP. Beta-endorphin was the only form of immunoreactivity detected in the NIL and hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of immobilization stress on beta-endorphin levels are modulated by testosterone. 297 25

In addition to corticotropin-releasing factor (CRF) and structurally related peptides, arginine vasopressin (AVP), oxytocin, angiotensin II, vasoactive intestinal polypeptide, peptide histidine isoleucinamide, epinephrine (E), and norepinephrine induce secretion of adrenocorticotropin (ACTH) from corticotropic cells in vitro. The apparent affinity and intrinsic ACTH-releasing activity of these substances are lower than those of CRF. These substances can also act synergistically with CRF. In this paper the role of catecholamines and AVP in the control of ACTH release is discussed. Infusion i.v. of E increases plasma ACTH and corticosterone to levels that are normally found during stress. E-induced stimulation of pituitary-adrenal activity is mediated by beta adrenoceptors and involves release of CRF, because it can be prevented by beta-adrenoceptor blockers and by destruction of CRF neurons (hypothalamic lesions), blockade of CRF release (chlorpromazine, morphine, and Nembutal), or administration of CRF antiserum. Although stress can cause a vast increase in plasma E, circulating E is not essential for the acute stress-induced release of ACTH because blockade of beta (or alpha) adrenoceptors, administration of chlorisondamine, or extirpation of the adrenal medulla and sympathectomy do not prevent the pituitary-adrenal response to stress. In contrast, circulating E plays a major role in the release of intermediate-lobe peptides during emotional stress. Studies of the role of AVP in pituitary-adrenal control by the use of pressor receptor (V1) antagonists are not valuable because of the ineffectiveness of such antagonists in blocking AVP-induced release of ACTH from corticotropic cells in vitro. Treatment of rats with an antiserum to AVP reduces the ACTH response to stress. We conclude that AVP has an important role in stress-induced activation of the pituitary-adrenal system, possibly by potentiating the effects of CRF.
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PMID:Role of epinephrine and vasopressin in the control of the pituitary-adrenal response to stress. 298 37

The effects of acute and chronic stress on the release of ACTH and beta-endorphin in response to stimulation by ovine corticotropin-releasing factor (CRF) and arginine vasopressin were examined. Pituitaries were removed from rats who had received either acute stress, chronic stress daily for 14 days with the last stress occurring 24 h before decapitation, or chronic stress followed by an acute stress immediately before decapitation (chronic stress-acute stress). Pituitaries from naive unstressed animals were used as the control group. After processing into single cell suspensions, the pituitaries were incubated with various doses of CRF (10(-11) M to 10(-9) M) and AVP (10(-10) M to 10(-8) M). Release of ACTH and beta-endorphin into the medium was measured by RIA. A clear dose-dependent response to both releasers was seen in control pituitaries. In acute stress, a decreased responsiveness to arginine vasopressin and CRF was seen. This same blunted response was not seen in chronic stress even if the animals are stressed immediately before decapitation. At higher doses of CRF (10(-9) M) a substantially increased release of ACTH and beta-endorphin was seen in the chronically stressed rats. When the content of the anterior pituitary lobe was assayed in these animals, both chronic stress groups show increased content of ACTH and beta-endorphin, which may indicate an increase amount of ACTH and beta-endorphin in the releasable pools in chronic stress. In addition, the failure of further stress to alter the response to CRF in the chronic stress-acute stress group may indicate a down-regulation of the steroid feedback on the pituitary. However, it is clear that no down-regulation of the CRF receptor occurs in this chronic stress paradigm.
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PMID:Corticotropin-releasing factor stimulation of adrenocorticotropin and beta-endorphin release: effects of acute and chronic stress. 298 16


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