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 release of adrenocorticotropin (ACTH) from the corticotrophs is controlled principally by vasopressin and corticotropin-releasing hormone (CRH). Oxytocin may augment the release of ACTH under certain conditions, whereas atrial natriuretic peptide acts as a corticotropin release-inhibiting factor to inhibit ACTH release by direct action on the pituitary. Glucocorticoids act on their receptors within the hypothalamus and anterior pituitary gland to suppress the release of vasopressin and CRH and the release of ACTH in response to these neuropeptides. CRH neurons in the paraventricular nucleus also project to the cerebral cortex and subcortical regions and to the locus ceruleus (LC) in the brain stem. Cortical influences via the limbic system and possibly the LC augment CRH release during emotional stress, whereas peripheral input by pain and other sensory impulses to the LC causes stimulation of the noradrenergic neurons located there that project their axons to the CRH neurons stimulating them by alpha-adrenergic receptors. A muscarinic cholinergic receptor is interposed between the alpha-receptors and nitric oxidergic interneurons which release nitric oxide that activates CRH release by activation of cyclic guanosine monophosphate, cyclooxygenase, lipoxygenase and epoxygenase. Vasopressin release during stress may be similarly mediated. Vasopressin augments the release of CRH from the hypothalamus and also augments the action of CRH on the pituitary. CRH exerts a positive ultrashort loop feedback to stimulate its own release during stress, possibly by stimulating the LC noradrenergic neurons whose axons project to the paraventricular nucleus to augment the release of CRH.
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PMID:Role of the hypothalamic pituitary adrenal axis in the control of the response to stress and infection. 1100 12

A variety of stressful events, including emotional stress, cause a marked increase in noradrenaline release in several brain regions, and especially in the hypothalamus, amygdala and locus coeruleus, in the rat brain. These findings suggest that an increased noradrenaline release could be closely related to the provocation of negative emotions such as anxiety and/or fear. In order to confirm this hypothesis, we carried out several studies. Diazepam, a typical benzodiazepine anxiolytic, significantly attenuated not only the immobilization stress-induced increase in noradrenaline release in the three rat brain regions but also the emotional changes of these animals, and these effects were antagonized by flumazenil, a benzodiazepine antagonist. Naloxone and opioid agents, such as morphine, beta-endorphin and [Met(5)]-enkephalin, significantly enhanced and attenuated the stress-induced increase in noradrenaline release in these regions and the stress-induced emotional change, respectively. Two stressful events which predominantly involve emotional factors, i.e., psychological stress and conditioned fear, caused significant increases in noradrenaline release selectively in these three brain regions and these increases were also significantly attenuated by pretreatment with diazepam in a flumazenil reversible manner. Yohimbine, an alpha(2)-adrenoceptor antagonist which caused a marked increase in noradrenaline release in the several brain regions, had an anxiolytic action in the two behavioral tests involving anxiety, i.e., the conditioned defensive burying test and the modified forced swim test. beta-Carbolines, which possess anxiogenic properties, significantly increased noradrenaline release in the hypothalamus, amygdala and locus coeruleus. Taken together, these findings suggest that the increased release of noradrenaline in the hypothalamus, amygdala and locus coeruleus is, in part, involved in the provocation of anxiety and/or fear in animals exposed to stress, and that the attenuation of this increase by benzodiazepine anxiolytics acting via the benzodiazepine receptor/GABAA receptor/chloride ionophore supramolecular complex may be the basic mechanism of action of these anxiolytic drugs.
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PMID:Noradrenaline systems in the hypothalamus, amygdala and locus coeruleus are involved in the provocation of anxiety: basic studies. 1103 44

To evaluate the role of opioids for the regulation of oxytocin release in response to teat stimulation, 10 brown-Swiss dairy cows were randomized to two experiments during mid of lactation. In the first experiment, four cows without previous suckling experience were suckled by an alien calf between two normal milkings. Before and during milking or suckling, frequent blood samples were collected via a jugular cannula for determination of oxytocin and beta-endorphin. In the second experiment, six cows were treated with naloxone or saline, 10min before the start of the first or second suckling, respectively. The collected blood samples were assayed for oxytocin.In the first experiment, the plasma levels of beta-endorphin were elevated during and after the unexperienced suckling in three cows, but not in the fourth cow, and the release of oxytocin during suckling was markedly reduced, suggesting no release of alveolar milk. In the second experiment, the release of oxytocin during suckling was again significantly reduced. Pretreatment with naloxone before suckling did not completely abolish the adverse effect of suckling and the oxytocin plasma level did not increase to levels comparable with control milking.In emotional stress situations, the release of oxytocin from the pituitary is inhibited with simultaneously elevated beta-endorphin plasma levels. Although there is some evidence for a regulatory role of opioids for the release of oxytocin, other mediators are suggested to be more potent in regulating oxytocin under stress conditions.
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PMID:Naloxone cannot abolish the lack of oxytocin release during unexperienced suckling of dairy cows. 1131 18

Psychological, endocrine and immune parameters were measured over a 6-month period in 14 healthy subjects who underwent an unpredictable acute emotional stress (e.g. sudden death of a loved one) compared with 14 controls who did not. Probands were profoundly stressed as assessed 10 days after bereavement by their scores on the Hamilton Rating Scales of Anxiety and Depression, adrenocorticotropin and cortisol plasma concentrations, and non-suppression in response to dexamethasone. Functional alterations of immune parameters, such as responsiveness of peripheral blood lymphocytes to mitogens, were found 40 days after bereavement. Despite a normal number of circulating lymphocyte subsets, the functional activity of natural killer (NK) cells was markedly reduced at day 40. Changes in the intracellular concentration of beta-endorphin in peripheral blood mononuclear cells correlated with anxiety and depression scores. Controls showed no changes in psychometric, endocrine and immune measures during the 6-month study. Cluster analysis revealed two groups of bereaved subjects with different patterns of immune and endocrine changes: (1) Five subjects, characterized by harm-avoidant temperament and long-lasting dysphoric mood, showed reduced responsiveness of peripheral blood lymphocytes to mitogens, decreased NK cell activity and non-suppression in response to dexamethasone that persisted for 6 months. (2) Nine subjects showed significant changes only during the early phase after bereavement. Our data suggest that the immunological consequences of stress do not simply overlap with psychological and endocrine alterations, and are particularly severe and long-lasting in a subgroup of subjects, indicating the importance of individual variability in the capacity to cope with stress.
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PMID:Long-term immune-endocrine effects of bereavement: relationships with anxiety levels and mood. 1465 49

Members of the corticotropin-releasing factor (CRF) family of peptides play pivotal roles in the regulation of neuroendocrine, autonomic, and behavioral responses to physical and emotional stress. In amphibian tadpoles, CRF-like peptides stimulate both thyroid and interrenal (adrenal) hormone secretion, and can thereby modulate the rate of metamorphosis. To better understand the regulation of expression and actions of CRF in amphibians we developed a homologous radioimmunoassay (RIA) for Xenopus laevis CRF (xCRF). We validated this RIA and tissue extraction procedure for the measurement of brain CRF content in tadpoles and juveniles. We show that the CRF-binding protein, which is highly expressed in X. laevis brain, is largely removed by acid extraction and does not interfere in the RIA. We analyzed CRF peptide content in five microdissected brain regions in prometamorphic tadpoles and juveniles. CRF was detected throughout the brain, consistent with its role as both a hypophysiotropin and a neurotransmitter/neuromodulator. CRF content was highest in the region of the preoptic area (POa) and increased in all brain regions after metamorphosis. Exposure to 4h of handling/shaking stress resulted in increased CRF peptide content in the POa in juvenile frogs. Injections of xCRF into prometamorphic tadpoles increased whole body corticosterone and thyroxine content, thus supporting findings in other anuran species that this peptide functions as both a corticotropin- and a thyrotropin (TSH)-releasing factor. Furthermore, treatment of cultured tadpole pituitaries with xCRF (100nM for 24h) resulted in increased medium content, but decreased pituitary content of TSHbeta-immunoreactivity. Our results support the view that CRF functions as a stress neuropeptide in X. laevis as in other vertebrates. Furthermore, we provide evidence for a dual hypophysiotropic action of CRF on the thyroid and interrenal axes in X. laevis as has been shown previously in other amphibian species.
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PMID:Expression and hypophysiotropic actions of corticotropin-releasing factor in Xenopus laevis. 1520 Oct 65

In our previous study, repeated stress in the neonatal period was found to slow habituation in the open field in adult rats. The objective of the present study was to investigate how chronic stress can affect habituation processes in the open field when occurring in adulthood. Animals were exposed to 1 week of immobilization on metal boards followed by 1 week of hypokinesis. After the stress procedure, rats were tested in the open field (once daily in 6-min sessions for four consecutive days). Immediately after the last open-field test, animals were decapitated. The rapidity of between- and within-session habituation was lower than in control rats. However, this lowering failed to be statistically significant compared with control rats. On the other hand, time latency to step down from an elevated platform was significantly increased in stress-exposed animals. Four days after the last stressful event, corticotropin-releasing hormone mRNA levels in the paraventricular nucleus were significantly increased, indicating a long-term activation of the hypothalamic-pituitary-adrenocortical axis. The results suggest that, in contrast to neonatal stress exposure, chronic emotional stress in adult rats does not represent a risk factor for the alteration of habituation processes.
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PMID:Effect of chronic emotional stress on habituation processes in open field in adult rats. 1524 Mar 69

Anxiety disorders are often associated with autonomic symptoms, including heart palpitations, sweating, elevation of body temperature and alterations of gastrointestinal motility. Some of the alterations observed in animals exposed to stress are analogous to changes in a number of physiological and endocrine parameters observed in anxious patients. With the purpose to guide further clinical studies in subtypes of anxious patients, etifoxine, a nonbenzodiazepine anxiolytic compound, was evaluated in two rat models of anxiety with measures of physiological manifestations: stress-induced hyperthermia (SIH) and conditioned-fear-stress-induced freezing behavior and activation of colonic motility. The sequential handling of animals induced a rise in body temperature attenuated by etifoxine (50 mg/kg IP). The emotional stress induced by fear to receive electric foot shocks is accompanied by freezing behavior and an increase of the frequency of ceco-colonic spike bursts: both parameters were reduced by etifoxine (25-50 mg/kg IP), independently of changes in pain perception and memory-related processes. In response to a stressful event, the stimulation of the corticotropin-releasing hormone (CRH) system is probably involved in the observed modifications of body temperature and colonic motility. It is hypothesized that stress-induced CRH activation is attenuated by the enhancement of the inhibitory GABAergic system activity associated with etifoxine. These findings will guide future evaluation of etifoxine in the treatment of selected anxious patients with altered autonomic symptomatology.
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PMID:Effects of etifoxine on stress-induced hyperthermia, freezing behavior and colonic motor activation in rats. 1545 55

A causative link between emotional stress and acne has long been postulated. There is mounting evidence that the molecular mechanism underlying this observation is related to the expression of receptors for several neuroendocrine mediators by the sebaceous gland. Recent and ongoing studies have indicated that human sebocytes express functional receptors for corticotropin-releasing hormone, melanocortins, beta-endorphin, vasoactive intestinal polypeptide, neuropeptide Y and calcitonin gene-related peptide. After ligand binding, these receptors modulate the production of inflammatory cytokines, proliferation, differentiation, lipogenesis and androgen metabolism in sebocytes. By means of their autocrine, paracrine and endocrine actions, these neuroendocrine factors appear to mediate centrally and topically induced stress towards the sebaceous gland, ultimately affecting the clinical course of acne.
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PMID:Neuroendocrine regulation of sebocytes -- a pathogenetic link between stress and acne. 1550 10

Agouti protein is a paracrine signaling factor modulating action of ACTH and alpha-MSH. Dominant mutation Ay causes ectopic, ubiquitous expression of Agouti protein in mice. It was shown that Ay mutation increased stress-induced hypothalamo-adrenal activity in male mice. There is a sex difference in the hypothalamo-pituitary-adrenal axis in rodents. The aim of this study was to test effects of ectopic overexpression of Agouti protein on pituitary-adrenal function in female mice. Female mice of C57Bl/6J strain with Ay mutation (Ay/alpha) and with mutation nonagouti (alpha/alpha; lack of Agouti protein) were used. Ay/alpha-females had an increased blood level of corticosterone and ACTH after 10-minute restriction as compared with alpha/alpha-females. The adrenal threshold sensitivity and reaction to exogenous ACTH in vivo suggests that increased corticosterone reaction to emotional stress is caused by increased pituitary stimulation.
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PMID:[Pituitary-adrenal function in female mice with mutation Agouti yellow (A(y))]. 1564 7

The author postulates a need of individual evaluation of experimental data characterizing emotional stress. In typical conflict situations inducing emotional stress, there are animals resistant or predisposed to disturbance of different physiological functions. Prognostic criteria of individual resistance of animals to stressors are presented. Stress resistance depends in large on neuromediators and neuropeptides content, in particular Substance P, a peptide responsible for delta-sleep, and beta-endorphin, in brain structures and peripheral tissues. It is emphasized that individual estimation of clinical indices of emotional stress is needed.
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PMID:[Individuality of emotional stress]. 1579 2


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