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)

Correlation coefficients between handling time and plasma corticosteroid concentration of White Leghorn hens were minimal when times varied from 43 to 161 sec (r = .17; P less than .05, df = 244), and no association was found when blood collection times exceeding 90 sec were omitted (r = -.02, df = 219). Handling times carried to specific endpoints of 30 and 60 sec indicated no difference, but times of 60, 120, 180, and 600 sec were associated with highly significant differences in corticosteroid levels that were inconsistent between genetic stocks. Strains selected for increased part-year egg mass responded less rapidly to handling than did unselected control strains. Confinement of hens for 4 to 6 hr in nests within their own pens caused increases of greater than 30% in corticosteroids as compared to samples obtained from hens caught directly from the floor. Neither floor pen vs. colony cage nor genetic stock differences were found for plasma corticosteroid levels of hens at a mean age of 55 weeks. Adrenocorticotropic hormone stimulation of 63-week-old hens caused an 8.5-fold increase in corticosteroids above basal but failed to elicit differential effects associated with environments or genetic stocks. Nevertheless, hens kept in floor pens had 10.8% higher survival in the laying house and exceeded colony-cage hens by more than 40% in hen-day egg mass for the final 10 weeks of a 40-week laying period.
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PMID:Corticosteroid levels in white Leghorn hens as affected by handling, laying-house environment, and genetic stock. 400 Oct 69

Excessive grooming in response to intracerebroventricular (ICV) ACTH1-24 was assayed following various doses of diazepam, chlordiazepoxide and flurazepam. Grooming scores were only affected by doses of the benzodiazepines higher than those that depressed locomotor activity. Similarly, diazepam did not affect excessive grooming induced by ICV beta-endorphin, nor did chronic chlordiazepoxide affect ACTH-induced grooming. By contrast similar doses of the benzodiazepines decreased the increased grooming score observed when mice were observed in a novel as opposed to the home cage. This result is consistent with the hypothesis that novel cage-induced grooming is caused by an increase in the ventricular content of ACTH or beta-endorphin, and that the benzodiazepines decrease or prevent this increase. It is not consistent with hypotheses of a functional antagonism between ACTH and benzodiazepines, at least insofar as the mechanisms involved in the production of grooming are concerned.
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PMID:Benzodiazepines decrease grooming in response to novelty but not ACTH or beta-endorphin. 611 85

Groups of monkeys either extensively pretrained to avoid shocks in a shuttlebox or with minimal prior experience were compared for plasma cortisol and beta-endorphin levels immediately following: (1) an exposure to the box with no shock, (2) the box providing repeated inescapable shocks or (3) a re-exposure to the box, again with no shock presentation. Mere exposure to the unfamiliar box elevated plasma cortisol just as much as exposure + shock did when inexperienced monkeys were tested. However, animals with a history of previously successful shock avoidance showed smaller elevations when exposed to the box alone, than they did when inescapable shock was received. Plasma beta-endorphin levels following shuttlebox exposure showed only a sporadic pattern of elevations in either inexperienced or pretrained monkeys. However, levels of beta-endorphin as determined under control conditions in the home cage were lower in pretrained animals, as were plasma levels of cortisol. The results indicate that behavioral factors may effect plasma cortisol and beta-endorphin following both acute and chronic shuttlebox experience.
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PMID:Shuttlebox avoidance in rhesus monkeys: effects on plasma cortisol and beta-endorphin. 630 15

Neurotoxic doses of monosodium glutamate were administered to neonatal male and female Sprague-Dawley rats for five days postpartum. The rats were tested at 6 months for alterations in two forms of activity--initial activity in an open field and overnight activity in a familiar cage. In comparison with age-, sex- and handling-matched littermate controls, experimental subjects exhibited increased open field behaviors and reduced overnight activity. Subsequent histology indicated marked reductions in arcuate and periarcuate cells which included but probably were not limited to beta-endorphin containing neurons. These findings indicate that neonatal MSG has long-term behavioral and neurological consequences, that some changes occur within behaviorally discrete systems, and that they may be associated with functional alterations within endogenous opioid systems, inter alia.
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PMID:Neonatal monosodium glutamate differentially alters two models of behavioral activity in conjunction with reduced hypothalamic endorphins. 631 4

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

Defensive burying behavior is a coping strategy in rodents in response to an aversive stimulus where fear will facilitate burying and treatment with anxiolytics will result in less burying. To test the hypothesis that endogenous corticotropin-releasing factor (CRF) is involved in the defensive burying response, the effects of an ICV CRF antagonist were tested on defensive burying behaviors as well as the plasma adrenocorticotropic hormone (ACTH) and plasma corticosterone response. Rats were allowed to self-administer one mild electric shock (1.0 mA) through a probe mounted on the wall of the home cage by briefly touching it. Following this shock, control rats typically display burying behavior, as defined as moving the bedding material toward and/or over the shock probe. A CRF antagonist, alpha-hel CRF9-41, was administered ICV (1, 5, and 25 micrograms) 1 min after they received the shock. The 5 micrograms dose of the CRF antagonist significantly attenuated the time spent in defensive burying compared to vehicle-treated controls. The 5 and 25 micrograms doses of alpha-hel CRF9-41 increased the latency to display defensive burying. However, the enhanced release of plasma ACTH and plasma corticosterone concentrations in the stressed animals was not significantly modified over the 15-min period by either of the three doses of CRF antagonist. The results suggest that endogenous CRF is involved in the expression of defensive burying behavior and that the brain CRF receptors modulating the behavioral response may be different from the CRF receptors modulating the hormonal response of defensive burying.
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PMID:Effect of corticotropin-releasing factor antagonist on behavioral and neuroendocrine responses during exposure to defensive burying paradigm in rats. 808 89

To understand some of the mechanisms underlying the neuroendocrine and neurochemical changes associated with aging, we administered the serotonin [5-hydroxytryptamine (5-HT)] releaser and reuptake inhibitor d-fenfluramine (d-FEN; 0.0, 0.2, or 0.6 mg/kg/day, p.o) for 30-38 days to young (4 months) and old (22 months) F344 male rats. Rats were stressed by placement into a novel open field (OF) for 20 min before sacrifice. Control animals were sacrificed immediately upon removal from their home cage (HC). Old rats exhibited less (p < 0.05) exploratory behavior than young rats, which was not altered by treatment with d-FEN. Old HC rats also had higher (p < 0.05) basal plasma levels of adrenocorticotropic hormone (ACTH) and prolactin (PRL) than young HC rats. Old OF rats showed higher (p < 0.05) levels of ACTH and corticosterone (CORT) than young OF animals. A stress-induced increase in PRL secretion was not observed in old rats. Subchronic low-dose d-FEN normalized the enhanced ACTH and CORT responses of old animals to novelty. In addition to these endocrine changes, stress-induced increases in medial frontal cortex (MFC) dopamine (DA) and norepinephrine (NE) turnover also were observed. The increase in NE turnover was greater (p < 0.01) in old than in young rats. d-FEN treatment blocked the stress-induced increase in MFC NE but not MFC DA turnover in both young and old rats. These data support a role for 5-HT and/or NE in some age-related neuroendocrine perturbations and suggest that increased 5-HT neurotransmission can normalize the hyperactivation of the hypothalamo-pituitary-adrenal axis of old male rats.
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PMID:Neuroendocrine and neurochemical responses to novelty stress in young and old male F344 rats: effects of d-fenfluramine treatment. 825

Research from our laboratory has demonstrated that the presentation of an aversive conditioned stimulus produces pronounced suppression of several in vitro measures of immune status. The present study was designed to evaluate the role of central corticotropin-releasing hormone (CRH) in the mechanisms mediating these conditioned effects. The aversive conditioned stimulus was a distinct environment that had previously been associated with electric footshock. Lewis rats received intraventricular administration of either buffered saline or a dose of the CRH-selective receptor antagonist alpha-helical CRH(9-41) (0, 0.5, 5, or 50 micrograms) prior to exposure to the aversive conditioned stimulus or home cage control treatment. The aversive conditioned stimulus produced decreases in splenic natural killer cell activity, splenocyte responsiveness to the mitogens concanavalin A (ConA), phytohemagglutinin (PHA), lipopolysaccharide (LPS), and the combination of ionomycin and phorbol myristate acetate (PMA), blood leukocyte responsiveness to ConA and PHA, and the production of interleukin-2 and interferon-gamma by activated splenocytes. The conditioned stimulus also produced an increase in plasma levels of corticosterone. Pretreatment with alpha-helical CRH(9-14) completely blocked the conditioned stimulus-induced suppression of natural killer cell activity. The CRH antagonist had no attenuative effect on the conditioned suppression of splenocyte or blood leukocyte proliferation in response to mitogens, or the production of interleukin-2 or interferon-gamma by activated splenocytes. There was also no effect of alpha-helical CRH(9-14) on the conditioned stimulus-induced increase in plasma corticosterone. These findings suggest that conditioned stimulus-induced suppression of natural killer cell activity is mediated by a mechanism that involves activity at central CRH receptors, and that this conditioned modulation is independent of HPA activation. Furthermore, these results indicate that the mechanisms involved in conditioned stimulus-induced suppression of proliferative or cytokine production responses are distinct from those involved in the modulation of natural killer cell activity.
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PMID:Corticotropin-releasing hormone is involved in conditioned stimulus-induced reduction of natural killer cell activity but not in conditioned alterations in cytokine production or proliferation responses. 855 20

The aim of this study is to investigate time-related changes in substance P (SP), beta-endorphin (BE), and corticosterone (CORT) levels due to DSIP aftereffects in the control and stress rats. Experiments were carried out on male Wistar and August rats. The SP and BE immunoreactivity in the hypothalamus and plasma samples was determined radioimmunologically. Blood CORT level was determined radioimmunologically. The rats were stressed at nighttime in special cages and tied by tails to the back side of the cage. The stress experiments were repeated for 12 hours for 5 days. There were 6 groups: 1. control animals, 2. stress animals, 3. rats that received DSIP in a dose of 60 nmol/kg one hour before decapitation, 4. rats in which DSIP was injected 24 hour before decapitation, 5. stressed rats in which DSIP was injected one hour before decapitation during the 5th exposure to stress, 6. stressed rats to which DSIP was injected 12 hours before the 5th exposure to stress, i.e., 24 hours before decapitation. Our experiments showed that DSIP administration induced marked changes in SP, BE, and CORT levels in hypothalamus and blood plasma. This suggests that the long-term stress-coping effect of DSIP depends on considerable changes in the level of other oligopeptides and hormones induced by DSIP. Evidently, DSIP triggers these processes inducing a cascade of interrelated molecular reactions radically different in animals with different resistance to emotional stress. This cascade of sequential reactions is different in Wistar and August rats differing by their resistance to emotional stress. DSIP administration stimulates the mechanism of resistance in August rats to a lesser extent than in Wistar animals.
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PMID:Delta-sleep-inducing peptide sequels in the mechanisms of resistance to emotional stress. 859 3

The model of sleep deprivation in rats by the platform method has been extensively studied in our laboratory as a possible animal model of mania. At the end of the period of sleep deprivation, the rat does not fall asleep as soon as it is returned to its home cage, but shows a period of wakefulness of about 30 min, during which the animal presents a cohort of symptoms that appear to mimic those present in idiopathic mania. In particular, during this period the animal displays insomnia, a high degree of hyperactivity, irritability, aggressiveness, hypersexuality and stereotypy. Haloperidol (0.2 mg/kg) was effective in reducing latency to sleep, while L-sulpiride was much weaker (< 50 mg/kg). The dopamine D1 receptor antagonist SCH 23390 exhibited an extremely high potency and efficacy in reducing sleep latency, a significant effect being observed with 3 micrograms/kg. The administration of the specific D1 receptor agonist SKF 38393 markedly prolonged the period of insomnia with the correlated behavioral syndrome. When lithium was added to the diet and consumed during the sleep deprivation period in adequate amounts to produce serum lithium levels of 0.7-1.0 mEq/l, sleep latency and locomotor activity were significantly reduced. The administration of naloxone (1-10 mg/kg) reduced the latency to sleep in a dose-related manner. By contrast, morphine (1 and 5 mg/kg, i.p.), beta-endorphin and [D-Ala2,D-Leu5]enkephalin (i.c.v., 2 and 1 micrograms, respectively) markedly prolonged the insomnia. The model not only represents a confirmation in the rat that sleep loss often precedes and may trigger a manic episode in man, but suggests that an opioid-dopamine interaction may play a pathogenetic role in mania.
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PMID:Sleep deprivation in the rat: an animal model of mania. 877 65


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