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 aim of this study was to investigate possible differences between calves with or without stereotypies concerning their behavioural reaction to an acute stress situation such as an open field and their behavioural and pituitary-adrenal responses to long-term tethering. Behavioural observations, open field tests, sampling for baseline adrenocorticotropic hormone (ACTH), and adrenocortical response tests after synthetic ACTH administration were made on 48 4- to 7-months-old dairy calves housed in tether stalls. Behavioural observations and blood sampling for baseline ACTH and cortisol determination after synthetic ACTH were repeated a year later in the same animals. Individual stereotypy levels showed a high correlation between calf values and heifer values (p < 0.001). Baseline ACTH in the calves was related to individual stereotypy levels (p < 0.05) in that the calves with higher stereotypy levels had lower ACTH values. The release of cortisol after injection of synthetic ACTH was considerably higher in the animals as heifers than when they were calves (p < 0.001). There was a relation between adrenocortical response to ACTH and stereotypy level in the heifers, showing that the higher the stereotypy level, the lower the cortisol response (p < 0.05). In the open field tests, the calves with the highest stereotypy levels moved around least but explored most. In conclusion, this study shows that growing dairy cattle with relatively high levels of oral stereotypies differ from individuals devoid of, or with low stereotypy levels, in behavioural response patterns to a short-term stressor such as an open field in adreno-cortical responses to exogenous ACTH and in baseline ACTH after 2 weeks of tethering.
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PMID:Relations between oral stereotypies, open-field behavior, and pituitary-adrenal system in growing dairy cattle. 974 93

Stress worsens certain disorders such as migraines or asthma, and has also been implicated in sudden myocardial arrest. It was previously shown that acute psychological stress by immobilization results in dura mast cell degranulation, an effect blocked by pretreatment with antiserum against corticotropin-releasing hormone (CRH). Moreover, CRH was recently shown to induce skin mast cell degranulation. The effect of psychological stress was investigated on rat cardiac mast cells, because their release of coronary constrictive and proinflammatory molecules contributes to myocardial ischemia and possibly arrhythmias. Immobilization of rats for 30 min induced maximal cardiac mast cell degranulation as evidenced by light and electron microscopy. This effect was inhibited by pretreatment with the "antiallergic" drug sodium cromoglycate (cromolyn), which is thought to act primarily through mast cell stabilization. Mast cell degranulation was also blocked by preincubation with antiserum against CRH and was partially inhibited by a CRH type-1 receptor selective antagonist. Sensory neuropeptides did not appear to influence this effect, but a nonpeptide neurotensin receptor antagonist blocked stress-induced cardiac mast cell degranulation. This finding supports the involvement of neuropeptide neurotensin which is present in the heart and is known to trigger mast cell degranulation. These results indicate acute stress could result in local CRH and nonpeptide neurotensin release which could contribute to myocardial pathophysiology through direct or indirect release of cardiac mast cell mediators.
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PMID:A neurotensin receptor antagonist inhibits acute immobilization stress-induced cardiac mast cell degranulation, a corticotropin-releasing hormone-dependent process. 976 51

Corticotropin releasing factor (CRF), a neuropeptide secreted by hypothalamic and extrahypothalamic neurons, is thought to mediate stress-related behaviors. The tension reduction hypothesis suggests that ethanol drinking reduces stress; that drinking is reinforced by this reduced stress; and that the probability of drinking therefore subsequently increases. CRF also decrease food intake, and might decrease ethanol drinking similarly. We addressed these hypotheses directly by assessing the effects of intracerebroventricular (i.c.v.) CRF upon ethanol drinking (1 h/day). Rats were provided drinking tubes containing ethanol solutions that were gradually incremented in concentration (from 2% to 8% w/v, over 38 days). Ethanol intakes remained stable, ranging from 0.4 to 0.5 g/kg per hour on average, and a two-bottle choice test revealed that ethanol was preferred reliably to water. Third-i.c.v. cannulae were surgically implanted and CRF or vehicle was acutely injected immediately prior to the sessions. CRF dose-dependently reduced ethanol intake by 31% (0.5 microg) and 64% (5.0 microg), and reduced 24-h food by 9% and 21%, respectively, but did not alter body weights. I.c.v. CRF reduced ethanol drinking despite any acute stress-like effects that may have been present. Hence, these data are inconsistent with the tension reduction hypothesis. On the other hand, our results support the concept that food intake and ethanol drinking may be mediated by similar mechanisms.
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PMID:Effects of third intracerebroventricular injections of corticotropin-releasing factor (CRF) on ethanol drinking and food intake. 976 50

Previous reports indicate that the central nucleus of the amygdala (CeA) stimulates adrenocorticotropin and corticosterone secretion, suggesting a role for this region in central hypothalamo-pituitary-adrenocortical (HPA) stress regulation. To evaluate this hypothesis, this study assessed the impact of CeA lesion on the response of hypophysiotrophic paraventricular nucleus (PVN) neurons to acute restraint and chronic unpredictable stress exposure. In contrast to previous reports, CeA lesions did not affect corticosterone or ACTH secretion induced by acute stress. Acute restraint increased PVN corticotropin releasing hormone (CRH) mRNA expression, increased the number of parvocellular PVN neurons expressing the co-secretagogue arginine vasopressin (AVP), and induced cFOS mRNA expression in the parvocellular PVN. However, there was no additional effect of CeA lesion on any measure of PVN activation. Chronic unpredictable stress exposure induced long-term activation of the HPA axis, noted by thymic involution, adrenal hypertrophy and increased PVN CRH mRNA expression. Stress-induced changes in thymus and adrenal weights were not affected by CeA lesion. Further, CeA lesion rats did not differ from controls in post-stress CRH mRNA expression. However, basal CRH mRNA expression was increased in the PVN of CeA rats, suggesting that the CeA plays a role in long-term inhibition of the PVN. The results of these studies are not consistent with the hypothesis that the CeA is necessary for stress-induced pituitary-adrenocortical activation. Rather, this region may play a stressor-specific modulatory role in regulation of HPA function.
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PMID:Hypothalamo-Pituitary-Adrenocortical Regulation Following Lesions of the Central Nucleus of the Amygdala. 978 50

The hippocampus plays an important role in central stress integration. The present study tests the hypothesis that the ventral subiculum, as a principal source of hippocampal efferents, is involved in co-ordination of hypothalamo-pituitary-adrenocortical and behavioural responses to cognitively-processed information. Basal hypothalamo-pituitary-adrenocortical activation appears to be normal in ventral subiculum lesion rats, as basal corticosterone and adrenocorticotropic hormone secretion, anterior pituitary pro-opiomelanocortin and type 1 corticotropin-releasing hormone receptor messenger RNA expression, adrenal and thymus weight, and splenic mitogen activity are not affected by lesion. Lesions of the ventral subiculum induce glucocorticoid hypersecretion following restraint stress or open field exposure, whereas responses to ether inhalation are unaffected. Interestingly, ventral subiculum lesion does not affect fast glucocorticoid negative feedback inhibition of restraint-induced adrenocorticotropic hormone release. Corticotropin-releasing hormone immunoreactivity is increased in the hypothalamic paraventricular nucleus of ventral subiculum lesion rats, and is differentially depleted by acute stress exposure (relative to sham-lesion rats). However, ventral subiculum lesion does not affect basal and stress-induced corticotropin-releasing hormone, arginine vasopressin and cFOS messenger RNA expression in paraventricular nucleus neurons. Behavioural analysis reveals that ventral subiculum lesion rats are hyper-responsive to open field exposure, showing decreased total ambulation and reduced incidence of central square entry. The results suggest that the ventral subiculum plays a specific role in integrating cognitively-processed stimuli (e.g., restraint and open field exposure) into appropriate neuroendocrine and behavioural responses to stress. Enhanced stress-induced glucocorticoid secretion and increased corticotropin-releasing hormone biosynthesis are likely due to removal of oligosynaptic inhibitory input to the paraventricular nucleus subsequent to ventral subiculum lesion.
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PMID:Ventral subiculum regulates hypothalamo-pituitary-adrenocortical and behavioural responses to cognitive stressors. 988 60

Animals prenatally exposed to ethanol typically exhibit hypothalamic-pituitary-adrenal (HPA) hyperresponsiveness to stressors. In contrast to previous studies that have investigated effects of prenatal ethanol exposure on HPA responses to acute or intermittent stressors, our study investigated HPA responses to a chronic continuous stressor, cold stress (4 degrees C for 0, 1, or 3 days). We tested the hypothesis that prenatal ethanol exposure would result in increased plasma corticosterone (CORT) and adrenocorticotropin (ACTH) responses and increased peptide [corticotropin-releasing factor and vasopressin] mRNA levels in the paraventricular nucleus (PVN) of the hypothalamus compared to that in control animals. In addition, CORT and ACTH responses were measured after exposure to an acute stressor (i.p. isotonic saline injection), superimposed during chronic cold exposure, to examine possible sensitization of the HPA response to the acute stress. Thus, blood samples were collected at the end of each of the three periods of cold exposure, either before (0 min) or 15 min after acute stress. The subjects were adult male and female Sprague-Dawley rat offspring from prenatal ethanol (E), pair-fed (PF), and ad libitum-fed control (C) treatment groups. Exposure to cold stress resulted in significant body weight loss in E males at 1 day and in both males and females of all prenatal treatment groups by 3 days of cold stress. Males in all prenatal groups also exhibited significant increases in adrenal weight:body weight ratios. Cold stress alone (0 min condition) increased CORT levels in E males and overall ACTH levels in E males and females compared to controls. ACTH levels were also higher overall in E compared to control males after acute stress (15 min condition). Sensitization of the CORT response to acute stress was observed in males but not females across all prenatal treatment groups. Corticotropin-releasing factor and vasopressin mRNA levels in the PVN were not significantly affected by prenatal treatment or chronic cold stress in either males or females. In contrast, both males and females displayed increases in PVN thyrotropin-releasing hormone (TRH) mRNA levels after cold stress. These data support and extend previous work demonstrating differential effects of prenatal ethanol exposure on HPA responsiveness of male and female offspring, and suggest that E males may be more vulnerable to the effects of chronic cold stress than E females.
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PMID:Effects of prenatal ethanol exposure on hypothalamic-pituitary-adrenal responses to chronic cold stress in rats. 1006 60

The locus coeruleus (LC) is a key brainstem region involved in arousal and is highly responsive to alerting/stressful stimuli, including those that activate the hypothalamic-pituitary-adrenocortical (HPA) axis. It is currently unclear whether the LC exerts any regulatory influence on the HPA axis and, consequently, on neuroendocrine responses to stress. The present studies were designed to test the hypothesis that the LC promotes HPA axis responses to acute and chronic stress. Adult male rats received bilateral (6-hydroxydopamine) lesions of the LC that produced severe cell loss in the LC and 80% depletion of noradrenaline in medial prefrontal cortex. Notably, lesions did not affect dopamine-beta-hydroxylase protein content in the parvocellular paraventricular nucleus (PVN), indicating a lack of collateral damage to other ascending noradrenergic pathways. LC lesions significantly reduced peak adrenocorticotropic hormone (ACTH) and corticosterone responses to 30 min acute restraint stress. However, LC lesions did not significantly attenuate neuroendocrine or other physiological responses to a 4-week chronic variable stress regimen. LC lesions did not substantially affect basal concentrations of plasma corticosterone or corticotropin-releasing hormone mRNA expression in the hypothalamic paraventricular nucleus following chronic stress. We conclude that the LC is a HPA-excitatory brain region, promoting neuroendocrine and physiological responses primarily to acute stress. However, a potential role for the LC in the induction of HPA axis hyperactivity following chronic stress can not be ruled out.
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PMID:Excitatory influence of the locus coeruleus in hypothalamic-pituitary-adrenocortical axis responses to stress. 1032 May 63

In response to stress, adrenocorticotropin (ACTH) is secreted from anterior pituitary corticotropes. Corticotropin-releasing hormone (CRH) is a potent stimulator of ACTH secretion. The CRH stimulation of secretion is mediated by cAMP and is largely dependent on Ca(2+) influx through voltage-gated L-type Ca(2+) channels. This study was designed to investigate whether the expression of L-type Ca(2+) channels in the rat anterior pituitary and in corticotropes is regulated by acute stress and CRH. RNase protection assays were used to quantify alpha(1C) mRNA of the L-type Ca(2+) channel. The alpha(1C) mRNA levels from stressed rats increased by 31% in anterior pituitaries of rats after 30 min of exposure to cold stress. Neither 60 min cold stress nor 30 min restraint stress had an effect on alpha(1C) mRNA levels. When alpha(1C) mRNA was detected by in situ hybridization in a population of corticotropes enriched to 90%, 0.5 nM CRH (3 h) stimulated a 36% increase in the average area of label/cell and a 10% increase in the average density of label. Our results suggest that (1) the expression of alpha(1C) subunit mRNA of L-type Ca(2+) channels is increased in the rat anterior pituitary with a stress-specific response that might reflect an increase both in thyrotropes and corticotropes (both are known to be stimulated by cold stress), and (2) the CRH-mediated increase in alpha(1C) mRNA expression in individual rat corticotropes, in vitro, supports the hypothesis that some of the increase in vivo is due to changes in corticotropes.
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PMID:Cold stress and corticotropin-releasing hormone induced changes in messenger ribonucleic acid for the alpha(1)-subunit of the L-type Ca(2+) channel in the rat anterior pituitary and enriched populations of corticotropes. 1042 89

Antalarmin is a pyrrolopyrimidine compound that antagonizes corticotropin-releasing hormone (CRH) type 1 receptors (CRHR1). In order to assess the effects of antalarmin treatment on hypothalamic-pituitary-adrenal (HPA) function we measured the plasma concentrations of adrenocorticotropic hormone (ACTH) and corticosterone in animals treated with either antalarmin or vehicle for 1 week or for 8 weeks. We found that antalarmin treatment for 1 week did not affect basal concentrations of ACTH or corticosterone. In contrast, treatment for 8 weeks significantly lowered basal ACTH and corticosterone concentrations and also significantly decreased the basal corticosterone to ACTH ratio, indicating decreased basal adrenocortical responsiveness to ACTH. However, immobilization stress resulted in ACTH and corticosterone concentrations that were the same in animals treated with vehicle or antalarmin for either 1 or 8 weeks. We conclude that even though 8-week antagonism of CRHR1 by the non-peptide antalarmin blunts basal concentrations of ACTH and corticosterone, and affects the adrenal responsiveness to ACTH, it does not blunt the HPA response to acute stress, and it does not appear to cause stress-induced adrenal insufficiency.
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PMID:Chronic administration of the non-peptide CRH type 1 receptor antagonist antalarmin does not blunt hypothalamic-pituitary-adrenal axis responses to acute immobilization stress. 1042 33

During early development, environmental challenges set the stage for permanent changes in the functioning of the pituitary-adrenal stress response. Since these data have been reported almost exclusively in single rat strains the role of phenotypic and genotypic factors in shaping the stress response is relatively unknown. This study examined whether the phenotypic/genetic profile of the rat influences the long-term response to challenge after early exposure to stress. Two strains of Sprague-Dawley rats were used in this study: one is a stress-induced animal model of "learned helpless" (LH) behavior and the other a resistant strain developed through selective breeding. Stress-induced adrenocorticotropic hormone (ACTH) and corticosterone release was monitored in adult congenital learned helpless (cLH) rats and congenital non-learned helpless (cNLH) rats. The rats were exposed to cold stress or maternal deprivation (on either postnatal day 7 or day 21). After the early acute stress exposure, animals remained undisturbed until challenged in adulthood (day 90) with footshock stress. In cLH animals (adults) early cold stress (particularly after acute stress on postnatal day 21) and maternal deprivation stress resulted in an enhancement of stress-induced ACTH release compared to nonstressed cLH and cNLH controls. In contrast, adrenal responsiveness was generally suppressed in cLH animals that were acutely stressed with cold stress or maternal deprivation stress early in life. The above results suggest that the genetic/phenotypic profile of the animal is a determinant in the changes observed in the adult stress response after early exposure to stressors.
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PMID:Early stress and genetic influences on hypothalamic-pituitary-adrenal axis functioning in adulthood. 1050 32


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