UNIPROT:P01189 - FACTA Search

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Query: UNIPROT:P01189 (beta-endorphin)
21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The neuropeptide galanin has been identified as a possible neurotransmitter/neuromodulator within the central nervous system. In the present study, a potential role for galanin in the lateral bed nucleus of the stria terminalis (BSTL) in modulating behavioral and neuroendocrine responses to an acute stress was investigated. In the first experiment, acute immobilization stress induced anxiety-like behavioral responses in rats, measured on the social interaction and elevated plus-maze tests. Immobilization stress decreased both social interaction time and open arm exploratory behavior on the elevated plus-maze. Bilateral administration of the galanin antagonist M40 (1.0 nmole/0.2 microl) into BSTL immediately prior to stress exposure attenuated the anxiogenic-like effects of immobilization stress, restoring both social interaction time and exploration of open arms to control levels. Administration of the antagonist alone had no effect on baseline behavior of unstressed control rats in either test, suggesting that the modulatory effect of galanin elicited during stress is not exerted tonically in unstressed animals. In the second experiment, immobilization stress produced an increase in plasma adrenocorticotropic hormone (ACTH) that was also attenuated by bilateral administration of M40 into BSTL prior to stress. These results suggest that during stress, the neuropeptide galanin exerts a modulatory effect in the BSTL, facilitating behavioral and neuroendocrine components of the acute stress response.
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PMID:Modulatory effects of galanin in the lateral bed nucleus of the stria terminalis on behavioral and neuroendocrine responses to acute stress. 1206 4

It is well known that stress affects the central nervous system (CNS), neuroendocrinoimmune system and other peripheral organs such as the gastrointestinal tract. However, the process of adaptation or recovery after acute stress reactions in these systems or organs during prolonged stress has not yet been adequately investigated. To clarify the process of adaptation or recovery in these systems and organs after acute stress reactions, the time course of these responses during a single long-duration restraint stress (RTS) was studied. The expression of c-fos in the hypothalamic paraventricular nucleus (PVN) region of the brain was induced and reached a peak at 0.5 hours for c-fos mRNA and 4 hours for c-fos protein (Fos), but disappeared at 2 hours for mRNA and 16 hours for Fos during continuous RTS. The activation of the hypothalamic-pituitary-adrenal (HPA) axis during stress resulted in rapid increases in the plasma levels of adrenocorticotropic hormone (ACTH) and corticosterone (CORT). Whereas the increase in ACTH was transient, the rise in CORT was maintained throughout the duration of the stress. A rapid significant decrease after stress exposure and following a slow and complete or partial recovery were observed in a number of total white blood cells (WBC), lymphocytes (LYM), helper T cells (Th) and cytotoxic/suppressor T cells (CTL/Ts). A gastric ulcer was found in 1/6 and 6/6 rats at 8 hours and 16 hours RTS, respectively. These results suggest that adaptive changes may occur in c-fos expression in the PVN, ACTH release and immune response, but not for CORT release, following acute stress reaction during long-duration RTS. In addition, any associated organic damage, such as gastric ulceration, was also suggested to possibly be progressive according to the duration of RTS.
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PMID:PVN c-fos expression, HPA axis response and immune cell distribution during restraint stress. 1206 82

Neuroendocrine activation during stress is affected by many factors contributing to the variability of the stress response. The present study was aimed at evaluating long-term changes in hypothalamo-pituitary-adrenocortical (HPA) axis function and in hedonic behavior in adult offspring prenatally stressed by maternal food restriction, with attention on possible gender differences. Adult offspring were blood sampled via a tail artery cannula. Prenatally stressed females had significantly higher adrenal weights compared to males. Plasma ACTH levels, which rose in response to acute stress induced by handling, were significantly higher in females compared to those in males. A similar pattern was found in plasma corticosterone. The rise in ACTH levels was more pronounced in prenatally stressed rats though the rise in corticosterone failed to be modified. Corticotropin releasing hormone (CRH) and proopiomelanocortin mRNA levels in the hypothalamic paraventricular nucleus and anterior pituitary, respectively, were found to be unchanged. The present experiments failed to reveal a decrease in hedonic behavior in prenatally stressed rats. In contrast, in male offspring a tendency to a higher sucrose preference was observed. These data together with observed changes in hormone and CRH mRNA levels indicate that the gestational stress used did not result in a depression-like state in adult offspring.
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PMID:Hypothalamo-pituitary-adrenocortical axis function and hedonic behavior in adult male and female rats prenatally stressed by maternal food restriction. 1218 80

Intestinal dysfunction is related to stress and early life events, but the mechanisms are largely unknown. Our aim was to determine whether early trauma predisposes adult rats to intestinal mucosal dysfunction in response to stress. Neonatal Sprague-Dawley rats were individually separated from their mothers for 3 h/day at 4-21 days of age. Between days 80 and 90, separated and control rats were subjected to mild acute stress (30-min water avoidance) or sham stress. Mucosal barrier function and ion transport were assessed in colonic tissues mounted in Ussing chambers. Mild stress increased short-circuit current, conductance, and transepithelial transport of macromolecules in separated rats, while having minimal effects in controls. Pretreatment of the separated rats with a corticotropin-releasing hormone (CRH) antagonist, the peptide alpha-helical CRH(9-41) injected intraperitoneally 20 min before stress, abolished the stress-induced mucosal changes. Our results indicate that neonatal trauma can induce phenotypic changes in adulthood, including enhanced vulnerability of the gut mucosa to stress via mechanisms involving peripherally located CRH receptors.
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PMID:Neonatal maternal separation predisposes adult rats to colonic barrier dysfunction in response to mild stress. 1238 89

Corticotropin-releasing factor (CRF) is involved in the regulation of stress responses. The actions of CRF in the brain are mediated through two distinct CRF receptor subtypes, CRF(1) and CRF(2) receptors. In the present study, we examined the effects in rat of chronic administration of a nonpeptidic CRF(1) receptor-selective antagonist, CRA1000, 2-[N-(2-methylthio-4-isopropylphenyl)-N-ethylamino]-4-[4-(3-fluorophenyl)-1,2,3,6-tetrahydropyridin-1-yl]-6-methylpyrimidine), on locomotor activity, feeding behavior and the hypothalamic-pituitary-adrenal axis. Chronic CRA1000 treatment significantly decreased locomotor activity in the dark phase of the diurnal cycle. However, chronic CRA1000 treatment showed no effect on food and water intake, or on body weight. After a 10-day period of CRA1000 treatment, plasma concentrations of adrenocorticotropic hormone (ACTH) and corticosterone in basal conditions and under immobilization stress were no different from those in rats treated with vehicle. However, CRA1000 administered 2 h before immobilization stress significantly reduced ACTH and corticosterone responses to stress with no effect on basal ACTH and corticosterone concentrations. These results suggest that CRF(1) receptors are involved in the regulation of locomotor activity during the dark period, but are not involved in the regulation of feeding behavior under non-stressful conditions. Furthermore, the results suggest that a 10-day treatment with CRA1000 does not affect hypothalamic-pituitary-adrenal axis activity either under basal conditions or after acute stress.
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PMID:Effect of chronic administration of a CRF(1) receptor antagonist, CRA1000, on locomotor activity and endocrine responses to stress. 1246 67

The hypothalamo-pituitary-adrenal (HPA) system is a most important mediator of the organism's response to stress. Secretory activity of this endocrine system displays a specific regulation during normal nocturnal sleep in humans. Pituitary release of adrenocorticotropin (ACTH) as well as adrenocortical release of cortisol decreases to a minimum during early sleep which is simultaneously characterized by maximum release of growth hormone (GH) and a predominance of slow wave sleep (SWS). In contrast, release of ACTH and cortisol reaches a maximum during late sleep which is simultaneously characterized by minimum plasma concentrations of GH and a predominance of rapid eye movement (REM) sleep. The nadir activity of the pituitary-adrenal system during early sleep reflects an active inhibition of this 'stress' system. One of the factors mediating this inhibition presumably is the sleep associated hypothalamic secretion of a release inhibiting factor of ACTH. In addition, limbic-hippocampal neuronal networks contribute to the inhibitory control over HPA activity during early sleep. Those structures appear to coordinate HPA inhibition and cortical activity (with prevalent SWS) during early sleep, thereby facilitating the formation of memories in sleep. As indicated by studies testing the effects of elevated plasma glucocorticoid levels, the inhibition of HPA activity during early sleep is an essential prerequisite for the memory function of sleep. Possibly, immunological memory formation likewise benefits from this inhibition. The suppression of pituitary-adrenal secretory activity during early sleep can be significantly weakened after profound acute stress as well as in states of chronic stress (including normal aging) which thereby disturb regular memory formation in sleep.
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PMID:The neuroendocrine recovery function of sleep. 1268 69

Many psychiatric disorders, including depression, post-traumatic stress disorder and other anxiety disorders, result from an interaction between genetic factors and exposure to a sufficiently sensitizing environmental stressor. The inbred Wistar Kyoto (WKY) rat strain has been proposed as a model of stress vulnerability, exhibiting an exaggerated hypothalamic-pituitary-adrenal (HPA) response to stress and susceptibility to gastric ulceration. Previously, we showed that stress-activation of the brain noradrenergic system was deficient in WKY rats, and they lacked noradrenergic facilitation of the HPA response in the lateral bed nucleus of the stria terminalis (BSTL), compared to outbred Sprague-Dawley (SD) controls. Deficient modulatory function of the noradrenergic system may contribute to the stress susceptibility of WKY rats. Thus, we investigated the influence of a sensitizing stimulus, chronic intermittent cold exposure, on neuroendocrine and noradrenergic stress reactivity, and on noradrenergic facilitation of the HPA response in these two strains. Chronic cold exposure (7 days, 4 h/day, 4 degrees C) potentiated activation of the HPA axis by acute immobilization stress, assessed by measuring plasma adrenocorticotropic hormone (ACTH), in both strains, although to a greater extent in WKY rats, and enhanced stress-induced norepinephrine (NE) release in BSTL of WKY but not SD rats. We then compared the influence of chronic cold exposure on noradrenergic modulation of the HPA stress response in BSTL, by measuring changes in acute stress-induced elevation of plasma ACTH after microinjecting the alpha(1)-adrenoreceptor antagonist benoxathian into the BSTL. As shown previously, benoxathian attenuated stress-induced ACTH secretion in control SD but not control WKY rats. After chronic cold, the ACTH response to acute stress was attenuated by benoxathian administration into BSTL of both strains, such that the WKY response was not different from that of SD rats. Thus, chronic cold not only sensitized the release of NE in BSTL of WKY rats, but also restored noradrenergic facilitation of their already-elevated HPA response. Such functional sensitization of a previously-deficient facilitatory system may be one mechanism whereby exposure to repeated or severe stress may induce pathologic dysregulation of the stress response in susceptible individuals, resulting in psychiatric illness.
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PMID:Chronic cold stress sensitizes brain noradrenergic reactivity and noradrenergic facilitation of the HPA stress response in Wistar Kyoto rats. 1269 37

The mechanisms that regulate neuronal function are a sum of genetically determined programs and experience. The effect of experience on neuronal function is particularly important during development, because early-life positive and adverse experience (stress) may influence the still "plastic" nervous system long-term. Specifically, for hippocampal-mediated learning and memory processes, acute stress may enhance synaptic efficacy and overall learning ability, and conversely, chronic or severe stress has been shown to be detrimental. The mechanisms that enable stress to act as this "double-edged sword" are unclear. Here, we discuss the molecular mediators of the stress response in the hippocampus with an emphasis on novel findings regarding the role of the neuropeptide known as corticotropin-releasing hormone (CRH). We highlight the physiological and pathological roles of this peptide in the developing hippocampus, and their relevance to the long-term effects of early-life experience on cognitive function during adulthood.
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PMID:Stress and the developing hippocampus: a double-edged sword? 1277 83

Stress is a ubiquitous and pervasive part of modern life that is frequently blamed for causing a plethora of diseases and other discomforting medical conditions. All higher organisms, including humans, experience stress in the form of a wide variety of stressors that range from environmental pollutants and drugs to traumatic events or self-induced trauma. Stressors registered by the central nervous system (CNS) generate physiological stress responses in the body (periphery) by means of the limbic-hypothalamic-pituitary-adrenal (LHPA) axis. This LHPA axis operates through the use of chemical messengers such as the stress hormones corticotropin-releasing hormone (CRH) and glucocorticoids (GCs). Under conditions of frequent exposure to acute stress and/or chronic, long-term exposure to stress, the LHPA axis becomes dysfunctional and in the process frequently overproduces both CRH and GCs, which results in many mild to severely toxic side effects. Bidirectional communication between the LHPA axis and immune/inflammatory systems can dramatically potentiate these side effects and create environments in the CNS and periphery ripe for the triggering and/or promotion of tissue degeneration and disease. This review aims to present as far as possible a molecular view of the processes involved so as to provide a bridge from the diffuse range of studies on molecular structure and receptor interactions to the burgeoning biological and medical literature that describes the empirical interplay between stress and disease. We hope that our review of this fast-growing field, which we christen chemical neuroimmunology, will give a clear indication of the striking range and depth of current molecular, cellular and medical evidence linking stress hormones to degeneration and disease. In so doing, we hope to provide encouragement for others to become interested in this critical and far-reaching field of research, which is very much at the heart of many important disease processes and very much a critical part of the crucial interface between chemistry and biology.
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PMID:Chemical neuroimmunology: health in a nutshell bidirectional communication between immune and stress (limbic-hypothalamic-pituitary-adrenal) systems. 1279 57

The role of vasopressin, cosecreted with corticotropin-releasing hormone (CRH), in stress is debated, because both normal as well as reduced adrenocorticotropin hormone (ACTH) rise to an acute challenge has been reported in Brattleboro rats genetically lacking vasopressin (di/di). Because di/di pups could be born either from di/+ (heterozygous) or from di/di mothers, and maternal influence is known to modify adult responsiveness, we investigated whether the influence of maternal genotype could explain the variability. Adult rats from mothers with different genotypes were stressed with 60 min restraint and trunk blood was collected for measuring hormone content by radioimmunoassay at the end of stress. All offspring of di/+ mothers had similar ACTH responses to restraint, while the di/di rats born to, and raised by di/di mothers showed reduced ACTH reactivity to restraint. The di/di rats showed elevated water turnover and required a daily cage cleaning every day, which meant frequent handling. To offset the role of handling, all rats had daily cage cleaning in the next series, but the results were the same as in the first series. To investigate whether lactation, the behaviour of the mother or some other factor during the pregnancy is responsible for the differences, pups from di/+ dams were raised by di/di foster mothers and vice versa. We found that the genotype of parental mother is more important than that of the foster mother. The corticosterone and prolactin elevation normally seen after acute stress was unchanged by family history, maternal or personal genotype. Furthermore, in studies with mutant animals, the rearing conditions should be controlled by the experimenter. In experiments with Brattleboro rats, the use of homozygous and heterozygous rats from the same litters of di/+ dams and di/di males is recommended. Our results suggest that vasopressin is not indispensable for ACTH release, and that the di/di genotype of the parental mother can decrease the stress reactivity of the di/di Brattleboro rats.
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PMID:Maternal genotype influences stress reactivity of vasopressin-deficient brattleboro rats. 1463 71

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