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)

Adult male Swiss-Webster (NIH) mice were isolated for 6 weeks. Aggressive behavior was tested on 2 occasions, 24 hours apart. Immediately following the 2nd test period, aggressors and isolated non-aggressors (controls) were decapitated and alpha-MSH concentration was measured in discrete areas of the brain. Only the nucleus accumbens and preoptic lateralis of the aggressors, showed a higher level of alpha-MSH when compared to the controls. The significance of these changes is discussed.
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PMID:Changes in alpha-melanotropin in discrete brain areas of isolated aggressive mice. 688 28

Earlier experiments demonstrated that the injection of alpha-melanocyte stimulating hormone into one mouse of a male pair results, 15 minutes later, in the release of an olfactory cue which increases the aggressive behavior of its partner. Because the preputial gland, whose activity is dependent upon testosterone and alpha-MSH, produces an odor which stimulates aggressive behavior, its relationship with the MSH response was investigated. Preputialectomy failed to prevent the release of the odor by an MSH-treated subordinate mouse of a pair, although preputialectomy of one mouse of a naive pair resulted in it later displaying higher levels of aggression than its intact partner, which then became subordinate. Swabs taken from the perineal region of alpha-MSH-injected subordinates, contained more aggression-promoting factor than swabs taken from saline injected subordinates. It is concluded that the short-term effects of alpha-MSH upon aggression are probably via a product of glandular or urinary origin other than the preputial gland and that the latter is more involved in long-term aggression-promoting cues.
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PMID:The source of an aggression-promoting olfactory cue, released by alpha-melanocyte stimulating hormone, in the male mouse. 719 71

The physiological effects of a psychosocial threat (the mere presence of a potentially antagonist individual in the home cage) were studied in aggressive and nonaggressive rats. Aggressive animals spent a significantly longer time with the investigation of the opponent compared with the nonaggressive group. An increase in plasma epinephrine and corticosterone was noticed both in aggressive and nonaggressive animals. Ir beta-endorphin increased significantly only in nonfighters. Glycemia was slightly larger in nonaggressives, while lactaemia increased in both groups. The possibility is discussed that differences in psychosocial stress response may be involved in the regulation of behavior in a real encounter.
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PMID:Hormonal and metabolic responses during psychosocial stimulation in aggressive and nonaggressive rats. 783 3

The present study was designed to investigate the coupling mechanisms linking the immune and the neuroendocrine corticotropic systems in an integrated defense response triggered by an infectious aggression. The experimental paradigm used consisted of the exploration in individual conscious rats of the temporal pattern of increased plasma concentrations of the two stress hormones, adrenocorticotropic hormone (ACTH) and corticosterone (Cort), and of three cytokines known as ACTH stimulators, tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1 beta, and IL-6, after intra-arterial infusions of lipopolysaccharide (LPS) given at three doses, 5 micrograms/kg (LPS-5), 25 micrograms/kg (LPS-25), and 1 mg/kg (LPS-1,000). Blood samples were taken 30 min and immediately before LPS injection (t0) and at 15, 30, 60, 120, 300, and 480 min post-LPS. The three doses of LPS induced ACTH and Cort surges, starting after 30 min for LPS-5 and LPS-25 or 15 min for LPS-1,000 and peaking with a similar amplitude at 60 min before receding slowly to baseline at 480 min for the two lower LPS doses. On the other hand, whatever the LPS dose, none of the three cytokines rose above undetectable basal levels before 60 min. They increased thereafter to culminate 10- to 30-fold above baseline at 60 min (TNF-alpha) or 120 min (IL-1 beta and IL-6) after LPS and declined back to basal levels at 300 min (TNF-alpha, all doses, and IL-6 for LPS-5 and LPS-25). After LPS-25, only IL-1 beta had not regressed to baseline levels at 480 min.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Temporal cascade of plasma level surges in ACTH, corticosterone, and cytokines in endotoxin-challenged rats. 804 20

Gastroesophageal reflux and pulmonary disease have become causally associated owing to reports of improved pulmonary function in patients with asthma or stridor following antireflux pharmacotherapy or surgery. Mechanisms by which reflux causes pulmonary disease include direct aspiration and neural reflex arcs. A novel additional mechanism for acute life-threatening episodes implicates increased beta-endorphin levels resulting from acid-mediated esophageal pain in the depression of respiratory drive. Diagnostic modalities used in the evaluation of reflux have often been inadequate to demonstrate a cause-and-effect relationship between reflux and pulmonary disease. Recent studies using multiple site pH-metry have attempted to provide evidence for cause and effect but have achieved mixed results. Aggressive antireflux pharmacotherapy and, sometimes, surgery help those patients with chronic pulmonary disease mediated by gastroesophageal reflux.
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PMID:Evaluation and management of gastroesophageal reflux and pulmonary disease. 881 96

The behavioral effects of alpha-MSH, MCH, and alpha-MSH + MCH were investigated in the ventromedial nucleus (VMN) and medial preoptic area (MPOA) (bilateral, 100 ng in 0.5 microliter). Infusion of alpha-MSH into the VMN increased aggressive behavior; in the MPOA it reduced exploration and increased anxiety. In both areas it stimulated sexual behavior. MCH also stimulated sexual behavior in the MPOA and VMN and had an anxiogenic effect in the MPOA. The effect of alpha-MSH on aggression and exploration was antagonized by MCH. When given together, the two peptides were mutually antagonistic on anxiety. This study indicates that MCH has central nervous system effects and may be a partial alpha-MSH agonist.
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PMID:Behavioral effects of alpha-MSH and MCH after central administration in the female rat. 882 27

A number of recent studies suggest that interleukin 1 beta (IL-1 beta) is a major mediator of hypothalamo-pituitary-adrenal (HPA) responses following infectious aggression. We investigated whether IL-1 beta mediates long-term changes in HPA activity and studied the cellular regulation of the anterior pituitary. To mimic chronically elevated IL-1 beta production thought to occur during infectious diseases, osmotic pumps (Alzet type) were implanted in the peritoneal cavity of male rats and hIL-1 beta was infused continuously at rates of 1 or 3 micrograms/day. Effects of hIL-1 beta action on plasma ACTH, beta-endorphin (beta-EP) and corticosterone (CORT) secretion and on anterior pituitary (AP), ACTH and beta-EP content were followed. In addition, hypothalamic (HT) CRH mRNA and in AP, CRH receptor (CRH-Rc) mRNA, POMC nuclear primary transcript RNA, POMC nuclear intermediate processing RNA and POMC nuclear and cytoplasmic mRNA were quantified using a highly sensitive solution hybridization nuclease protection assay. Continuous infusion of hIL-1 beta stimulated the HPA axis at varying degrees. Increased HT CRH gene expression, AP POMC gene transcription, ACTH and beta-EP release occurred only during the first 3 days of the treatment. A long-lasting enhancement of ACTH and beta-EP synthesis and of POMC gene expression resulted from activated POMC gene transcription followed by an increased POMC mRNA stability and decreased POMC mRNA turnover. In the AP, stimulation of ACTH and beta-EP secretion and POMC gene transcription disappeared after continuous IL-1 beta treatment, possibly in part due to a refractory process mediated by decreased CRH-Rc gene expression in corticotropes.
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PMID:Effects of continuous infusion of interleukin 1 beta on corticotropin-releasing hormone (CRH), CRH receptors, proopiomelanocortin gene expression and secretion of corticotropin, beta-endorphin and corticosterone. 903 74

There is increasing abuse of androgenic anabolic steroids (AAS) by non-athletes. AAS abuse has been associated with psychiatric symptoms such as mania, major depression and aggression and the development of dependence. Little is known about the effects of AAS on hypothalamic-pituitary-adrenal axis function or corticotropin releasing factor, which may be involved in mediating some of the psychiatric symptoms associated with AAS abuse. Male Sprague-Dawley rats received one daily intra-muscular injection of the AAS nandrolone decanoate (ND, 15 mg/kg) or vehicle for 3 days. Animals were sacrificed either 1 h or 24 h after the last injection, brain regions dissected and trunk blood collected. Corticotropin releasing factor (CRF), CRF receptor1 (CRF-R1) and proopiomelanocortin (POMC) mRNAs were measured with solution hybridization/RNase protection. Circulating levels of corticosterone and adrenocorticotropin hormone (ACTH) were determined using radioimmunoassays. One hour following the last injection, ND significantly increased circulating levels of both corticosterone and ACTH levels. In the amygdala, CRF mRNA levels were unchanged 1 h after the last injection of ND but were significantly reduced at 24 h. The same was found for hypothalamic POMC. No significant AAS effects were observed on: hypothalamic CRF mRNA; POMC mRNA in the amygdala or CRF R1 mRNA in the anterior pituitary.
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PMID:Effects of the androgenic anabolic steroid, nandrolone decanoate, on adrenocorticotropin hormone, corticosterone and proopiomelanocortin, corticotropin releasing factor (CRF) and CRF receptor1 mRNA levels in the hypothalamus, pituitary and amygdala of the rat. 1077 31

In order to study neuroendocrine and behavioural stress responses in female rats post partum we aimed to establish a relevant emotional stressor -- the maternal defence test based on maternal aggression of a lactating resident towards a virgin or lactating intruder approaching the cage. Exposure to maternal defence significantly elevated corticotropin (ACTH) and corticosterone responses of the residents and of virgin or lactating intruders, with an attenuated response in lactating residents and lactating intruders. Exposure to maternal defence increased plasma oxytocin in virgin intruders only. The aggressive behaviour displayed by the residents was directly correlated with the amount of defensive behaviour of the intruder and independent of the intruder's reproductive state. However, the amount of maternal and explorative behaviours displayed by the lactating residents was significantly higher when exposed to a lactating, compared to a virgin, intruder. ACTH responses in lactating residents exposed to virgin intruders were significantly correlated to the amount of offensive (direct correlation) and maternal (inverse correlation) behaviours they displayed. Plasma prolactin concentrations, elevated in lactating compared to virgin rats under basal conditions, were found to be reduced in the lactating residents and intruders in response to exposure to the maternal defence test, whereas it was unchanged in virgin intruders. To test for the involvement of brain oxytocin in neuroendocrine and behavioural responses of the lactating residents an oxytocin receptor antagonist (0.1 microg/5 microL) was infused icv 10 min prior to testing. This treatment increased basal, but not stress-induced, ACTH, corticosterone and oxytocin secretion. Whereas parameters of aggressive behaviour were unchanged, the antagonist reduced signs of maternal behaviour during maternal defence. In summary, the maternal defence test has been characterized as a relevant emotional stressor for female rats which is useful for studying neuroendocrine and emotional responses in females, in particular in the context of reproductive adaptations.
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PMID:Maternal defence as an emotional stressor in female rats: correlation of neuroendocrine and behavioural parameters and involvement of brain oxytocin. 1126 75

Childhood conduct disorder (CD) may originate in a stressful upbringing, and be associated with unusual physical or sexual development and thyroid dysfunction. We therefore explored circulating levels of hormones from adrenal, gonadal and growth hormone axes associated with stress, aggression and development in 28 CD patients and 13 age-matched healthy children (10-18 years old). The CD group had higher levels of dehydroepiandrosterone sulphate (DHEA-S), corticotropin (ACTH) and free tri-iodothyronine (fT(3)) if under 14 years. There were no differences for gonadal hormones or maturity ratings which were not associated with aggression. Smaller physical measures in CD children correlated with DHEA-S and growth factors (e.g. insulin-like growth factor I) increased ACTH and fT(3) correlated with restless-impulsive ratings, and DHEA-S with 'disruptive behaviour'. Imbalances in the adrenal and growth axes may have neurotropic repercussions in development.
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PMID:Dehydroepiandrosterone sulphate and corticotropin levels are high in young male patients with conduct disorder: comparisons for growth factors, thyroid and gonadal hormones. 1128 91


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