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)

Prolactin (PRL) has been shown to promote maternal behaviour, and to regulate neuroendocrine and emotional stress responses. These effects appear more important in the peripartum period, when the brain PRL system is highly activated. Here, we studied the mechanisms that underlie the anti-stress effects of PRL. Ovariectomized, estradiol-substituted Wistar rats were implanted with an intracerebroventricular cannula and treated with ovine PRL (0.01, 0.1 or 1 microg/h; 5 days via osmotic minipumps) or vehicle, and their responses to acute restraint stress was assessed. Chronic PRL treatment exerted an anxiolytic effect on the elevated plus-maze, and attenuated the acute restraint-induced rise in plasma adrenocorticotropin, corticosterone and noradrenaline. At the neuronal level, in situ hybridization revealed PRL effects on the expression patterns of the immediate-early gene c-fos and corticotropin-releasing factor (CRF). Under basal conditions, PRL significantly reduced c-fos mRNA expression within the central amygdala. In response to restraint, the expression of both c-fos mRNA and protein and of CRF mRNA was decreased in the parvocellular part of the paraventricular nucleus (PVN) of PRL-treated compared with vehicle-treated animals. In conclusion, our data demonstrate that chronic elevation of PRL levels within the brain results in reduced neuronal activation within the hypothalamus, specifically within the PVN, in response to an acute stressor. Thus, PRL acting at various relevant brain regions exerts profound anxiolytic and anti-stress effects, and is likely to contribute to the attenuated stress responsiveness found in the peripartum period, when brain PRL levels are physiologically upregulated.
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PMID:Chronic intracerebral prolactin attenuates neuronal stress circuitries in virgin rats. 1743 67

Neurons producing melanocortin receptor agonist, alpha-MSH derived from proopiomelanocortin, and antagonist, agouti-related protein, are known to be sensitive to metabolic stress such as food deprivation and glucoprivation. However, how these neurons respond to emotional/psychological stress remained to be elucidated. We report here that acute emotional stressors, i.e. restraint and forced swim, evoked mRNA expression of c-fos, a neuronal activation marker, in a high percentage of proopiomelanocortin neurons (up to 53% for restraint stress and 62% for forced swim), with marked variations along the rostro-caudal axis of the arcuate nucleus. In contrast, only a small population of agouti-related protein neurons in this brain region was activated. These neuronal activation patterns were correlated with behavioral reactions. Both stressors suppressed feeding and induced anxiety-like behavior in the elevated plus-maze test, as reflected by a reduction in the percentage of entries and time spent in the open arms. Central pretreatment with SHU9119, a melanocortin receptor antagonist, dose dependently attenuated the anorectic and anxiogenic effects elicited by acute restraint or forced swim. These results indicate that the melancortinergic pathway can be rapidly recruited by acute emotional stress, and that activation of melanocortin signaling is involved in mediating stress-induced anorexia and anxiety.
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PMID:The melanocortinergic pathway is rapidly recruited by emotional stress and contributes to stress-induced anorexia and anxiety-like behavior. 1767 12

It is established that pretreatment with Leuzea carthamoides extract (LCE) (1 ml/kg per os during 8 days) prevents the development of stress-induced (6-hr painful-emotional stress) damage of the rat heart. A chronic administration of LCE (1 ml/kg per os during 8 days) increased the cardiac tolerance to the cardiotoxic action of D, L-isoproterenol and the arrhythmogenic action of epinephrine. Pretreatment with naloxone (2 mg/kg) completely eliminated the cardioprotective effect LCE and attenuated but not abolished the antiarrhythmic effect of the phytoadaptogen. A chronic administration of LCE elevated the level of beta-endorphin levels in the rat blood plasma. It is suggested that the cardioprotective effect of LCE is related to an increase in the level of opioid peptides, which produce stimulation of the opioid receptors. It is also established that preliminary chronic administration of Aralia mandshurica extract (AME) increases the cardiac resistance to the arrhythmogenic action of a 45-min coronary artery occlusion, but has no effect on the necrosis/risk area ratio. A pretreatment with Eleutherococcus senticosus extract (ESE) (1 ml/kg per os during 8 days) prevented the stress-induced damages of the rat heart. A chronic administration of ESE increased the cardiac tolerance to the cardiotoxic action of D, L-isoproterenol and the arrhythmogenic action of epinephrine. The pretreatment with naloxone (2 mg/kg) completely eliminated both the cardioprotective action and the antiarrhythmic effect of the phytoadaptogen. A chronic administration of ESE increased the beta-endorphin level in the rat blood plasma. It is suggested that the cardioprotective and antiarrhythmic effects of ESE is also related to an increase in the endogenous opioid peptide levels. A chronic administration of ESE had no effect on the arrhythmogenic effect of a 45-min coronary artery occlusion and did not change the necrosis/risk area ratio in rats.
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PMID:[Cardioprotective and antiarrhythmic properties of preparations from Leuzea carthamoides, Aralia mandshurica, and Eleutherococcus senticosus]. 1831 96

New aspects of the classical Selye stress theory are considered. Stress is interpreted as a systemic response of the organism. In the last years the stress concept h as undergone transformation to the notion of emotional stress. In the context of the theory of functional systems, emotional stress is regarded as developing in the so-called conflict situations in which the participating subjects are unable to achieve useful adaptive goals. The primary cerebral mechanisms of emotional stress and the role played by neuromediators and neuropeptides are discussed. Dynamics of impairment of various functional systems under stressful conditions is discussed with special emphasis on individual tolerance to emotional stress and the role of oligopeptides (substance P), delta sleep inducing peptide, beta-endorphin and semax as antistress factors increasing resistance to stressful impacts.
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PMID:[Evolution of the stress concept]. 1914 Apr 65

Corticotropin releasing factor (CRF) is a neuropeptide that is a major regulator of the hypothalamic-pituitary-adrenal system. Recent findings have shown that CRF exists in extrahypothalamic areas in the brain as well as in the hypothalamus, and extrahypothalamic CRF is also deeply involved in stress responses. Therefore, CRF has been a major target of drug development for treatment of stress-related disorders. However, whether CRF is a cause or a result of fear/anxiety has not been investigated extensively, even though this issue is extremely important to the development of treatments for stress-related disorders. This article aims to 1) introduce readers to several functional aspects of CRF, focusing on aspects that have been missed or ignored when determining the roles of CRF in responses to emotional stress; 2) critically review previous studies regarding the roles of CRF in responses to emotional stress, considering functional aspects of CRF described in 1); and 3) put forward a hypothesis about the roles of CRF in stress responses. Considering different functional aspects of CRF, it was suggested that CRF is a result of fear/anxiety, rather than a cause. In other words, CRF could be responsible for stress responses to cope with dangerous situations but not for fear/anxiety itself. CRF as a potential target of drug development for treatment of stress-related disorders is also discussed.
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PMID:The roles of corticotropin releasing factor (CRF) in responses to emotional stress: is CRF release a cause or result of fear/anxiety? 1981 47

Hypothalamic-pituitary-adrenal (HPA) activity is altered postpartum and has been associated with several puerperal disorders. However, little is known about the association of maternal HPA activity during pregnancy with maternal HPA responsiveness to stress after parturition. Within a longitudinal study with an experimental component, we assessed in 22 women the salivary cortisol awakening response (CAR) at the 36th week of gestation and 6 weeks postpartum, as well as pituitary-adrenal and emotional responses to a psychosocial laboratory stressor at 8 weeks postpartum. CAR in late pregnancy negatively predicted maternal adrenocorticotropin (ACTH; ss = - 0.60; P = 0.003), plasma cortisol (ss = - 0.69, P < 0.001), and salivary cortisol (ss = - 0.66; P = 0.001) but not emotional stress reactivity (all P>0.05) at 8 weeks postpartum, whereas CAR at 6 weeks postpartum failed to predict hormonal (ACTH: ss = 0.02; P = 0.933, plasma cortisol: ss = - 0.23; P = 0.407, salivary cortisol: ss = - 0.15; P = 0.597) or emotional (all P>0.05) stress responses at 8 weeks postpartum. The activity of the HPA axis during pregnancy is associated with maternal HPA responsiveness to stress postpartum. Putative biological underpinnings warrant further attention. A better understanding of stress-related processes peripartum may pave the way for the prevention of associated puerperal disorders.
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PMID:Maternal cortisol in late pregnancy and hypothalamic-pituitary-adrenal reactivity to psychosocial stress postpartum in women. 2021 37

The aim of the work was to study effect of peripheral administration of mu-opioid receptor ligands unable to penetrate through the hematoencephalic barrier on the measures of emotionality in rats and on the release of beta-endorphins from nerve endings of the anterior cingulate cortex during emotional stress. The mu-opioid receptor agonist loperimide mostly acted as an anxiolytic whereas the receptor antagonist methylnaloxon showed depressive activity. Lifetime microdialysis and subsequent immunoenzyme assay demonstrated that intraventricular infusion of loperamide and methylnaloxon decreased and increased respectively the surge of beta-endorphin into the intercellular space. Immobilization-induced emotional stress insignificantly increased the beta-endorphin level in the cingulate cortex. Peripheral administration of loperamide but not methylnaloxon markedly increased the release of the neuropeptide during stress. These findings confirm the hypothesis of the authors about reciprocal interaction of central and peripheral components of the endogenous opioid system and explain the mechanism of antistress action of loperamide.
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PMID:[Central and peripheral mu-opioid systems in the mechanisms of emotional stress]. 2154 32

Housing mice in the presence of small particles of titanium has been shown to reduce stress-responsive behavior via the autonomic nervous system. Here, we examined the effects of nighttime titanium exposure on stress parameters and autonomic nerve activity in office workers with emotional stress. A randomized double-blind, placebo controlled trial was performed in 24 male subjects with desk jobs, who were randomly allocated to spend 5 nights in rooms with or without titanium. The serum concentrations of stress-responsive hormones (cortisol, adrenocorticotropin, and catecholamine) were measured, and profiles of emotional stress were collected to subjectively assess relaxation. Autonomic nerve activity was examined by power spectra analysis of heart rate variability. In psychological tests, factors related to tension (-14.5%, 95% CI=-15.7--2.1), anger (-11.3%, 95% CI=-13.9--0.7), and emotional stress (-28.5%, 95% CI=-30.0--5.3) were significantly decreased by exposure to titanium. The serum level of adrenocorticotropin was gradually elevated throughout the experimental period in the placebo group (day 4, 80.5%, 95% CI=7.1-37.5 vs. before trial) but not the titanium group. Power spectral analysis of R-R interval data showed a significant elevation in the high-frequency power spectral ratio in subjects housed in titanium rooms (days 1-2, 14.3%, 95% CI=4.7-21.9; days 3-4, 26.8%, 95% CI=4.9-38.7; and days 5-6, 24.1%, 95% CI=5.8-34.0 vs. before trial). These results suggest that sleeping in a room containing titanium lowers physiological and psychological stress.
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PMID:Titanium-treated surroundings attenuate psychological stress associated with autonomic nerve regulation in office workers with daily emotional stress. 2301 90

The prevalence of obesity is increasing worldwide with serious consequences such as diabetes mellitus type 2 and cardiovascular diseases. Emotional stress is considered to be one of the main reasons of obesity development in humans. However, there are some contradictory results, which should be addressed. First of all stress induces anorexia, but not overeating in laboratory animals. Glucocorticoids, the effector molecules of the hypothalamo-pituitary-adrenocortical (HPA) axis stimulate and stress inhibits food intake. It is also not clear if stress is diabetogenic or an antidiabetogenic factor. The review will discusses these issues and the involvement of the whole HPA axis and its separate molecules (glucocorticoids, adrenocorticotropin, corticotropin-releasing hormone) in food intake regulation under stress.
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PMID:Food-intake regulation during stress by the hypothalamo-pituitary-adrenal axis. 2359 Sep 31

Periodontal disease involves inflammation of the gingival tissues, caused by microbial pathogens. Recent papers suggest that emotional stress worsens periodontal disease. Here we review the literature and propose that corticotropin-releasing hormone (CRH) secreted under stress stimulates gingival mast cells together with other neuropeptides and cytokines to secrete pro-inflammatory molecules that contribute to periodontal pathology. Stress reduction and/or mast cell inhibition may provide additional therapeutic approaches.
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PMID:Stress hormones regulate periodontal inflammation. 2415 31


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