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)

Although the convergence of neural and humoral afferent information onto paraventricular neuroendocrine corticotropin-releasing hormone (CRH) neurons is a major determinant for adaptive stress responses, the underlying integrative mechanisms are poorly understood. To dissect the relative contributions made by neural afferents and corticosterone to these processes, we determined how the concurrent application of two heterotypic physiological stressors, chronic dehydration (produced by drinking hypertonic saline) and sustained hypovolemia (produced by subcutaneous injections of polyethylene glycol), is interpreted by the synthetic and secretory activity of CRH neurons using in situ hybridization and plasma ACTH measurements. These two stressors are encoded by relatively simple, distinct, and well defined sets of neural afferents to CRH neurons. Both increase plasma corticosterone, but they have opposing actions on CRH gene expression when applied separately. In the first experiment, we showed that chronic dehydration suppresses CRH gene transcription after hypovolemia, but not the preproenkephalin and c-fos mRNA responses or ACTH secretion. In the second, we showed that negative feedback actions of corticosterone do not suppress CRH gene activation after hypovolemia, but instead determine the prestress lower limit of a range within which the CRH gene then responds. Collectively, these data show that at least two processes are integrated to control how the CRH gene responds to multiple stimuli. First, the presence of corticosterone, which although permissive for appropriately activating the CRH gene during hypovolemia, does not mediate the suppressed gene response. Second, neural afferent-driven processes that encode dehydration play a central role in suppressing CRH activation.
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PMID:Interactions between heterotypic stressors and corticosterone reveal integrative mechanisms for controlling corticotropin-releasing hormone gene expression in the rat paraventricular nucleus. 1212 87

Intracerebroventricular (ICV) injection of prolactin-releasing peptide (PrRP) is known to increase plasma adrenocorticotropin (ACTH) and cause c-fos expression in the hypothalamic paraventricular nucleus (PVN). We hypothesize that this is the site at which PrRP acts to increase plasma ACTH. We have used ICV injection and direct intranuclear injection of PrRP into the PVN to investigate the sites important in the stimulation of ACTH release in vivo. To investigate the mechanism of action by which PrRP increases ACTH, we have used primary culture of pituitary cells and measured neuropeptide release from in vitro hypothalamic incubations. ICV administration of PrRP increased plasma ACTH 10 min post-injection (PrRP 5 nmol 81.0 +/- 23.5 pg/ml vs. saline 16.8 +/- 14.1 pg/ml, p < 0.05). Intra-PVN injection of PrRP increased ACTH 5 min post-injection (PrRP 1 nmol 22.9 +/- 5.0 pg/ml vs. saline 10.3 +/- 1.4 pg/ml, p < 0.05). This effect continued until 40 min post-injection (PrRP 1 nmol 9.9 +/- 1.5 pg/ml vs. saline 6.2 +/- 0.5 pg/ml, p < 0.05). In vitro PrRP (1-100 nmol/l) did not effect basal or corticotropin-releasing hormone (CRH)-stimulated ACTH release from dispersed anterior pituitary cells. PrRP increased hypothalamic release of CRH (PrRP 100 nmol/l 1.4 +/- 0.2 nmol/explant vs. the basal 1.1 +/- 0.2 nmol/explant, p < 0.05) but not arginine vasopressin. PrRP also stimulated neuropeptide Y release (PrRP 100 nmol/l 56.5 +/- 11.8 pmol/explant vs. basal 24.0 +/- 1.9 pmol/explant, p < 0.01), a neuropeptide known to stimulate the hypothalamo-pituitary-adrenal axis. Our data suggest that in vitro PrRP does not have a direct action on the corticotrope but increases plasma ACTH via the PVN and this effect involves the release of hypothalamic neuropeptides including CRH and neuropeptide Y.
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PMID:Prolactin-releasing peptide releases corticotropin-releasing hormone and increases plasma adrenocorticotropin via the paraventricular nucleus of the hypothalamus. 1216 68

In the fetal sheep, parturition is triggered by an increase in the activity of the fetal hypothalamus- pituitary-adrenal (HPA) axis which, in turn, augments the biosynthesis of oestrogen by the placenta. Parturition can be prevented or delayed by destruction of the paraventricular nucleus (PVN), pituitary or adrenal, or stimulated by infusions of adrenocorticotropin (ACTH) or glucocorticoids. We have previously reported that physiological increases in fetal plasma concentrations of oestradiol have a neuroendocrine effect to increase both basal and hypotension-stimulated ACTH secretion. The present study was performed to test the effect of oestradiol on the central baroreceptor and chemoreceptor reflex pathways. We used immunohistological techniques to identify various neuroanatomical regions which are activated by hypotension and, subsequently, those areas modified by oestrogen's action and baroreceptor and chemoreceptor denervation. We assessed cellular activation in these brain regions by immunostaining for Fos, the protein product of c-fos, an immediate early response gene. We found that oestradiol increased Fos abundance in nucleus tractus solitarius (NTS), rostral ventrolateral medulla (RVLM), and PVN, and augmented the increase in Fos in these regions in response to a 10 min period of brachiocephalic arterial occlusion (BCO). Carotid sinus denervation blocked the Fos response to BCO, but not to oestrogen alone, in these regions. In contrast, the hippocampus responded to BCO with increase Fos in intact fetuses, but did not respond to oestrogen treatment. None of the treatments altered Fos expression in cerebral cortex or in cerebellum. We conclude that oestradiol augments the activity of the central baroreceptor and chemoreceptor reflex pathways, and that it may influence fetal ACTH secretion via this site of action.
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PMID:Oestrogen augments the fetal ovine hypothalamus- pituitary-adrenal axis in response to hypotension. 1241 34

It has been reported that animals exposed to prior stress exhibit enhanced, reduced or equivalent hypothalamic-pituitary-adrenal (HPA) response to a subsequent acute stressor. We demonstrated previously that a long-duration restraint stress (RTS) evoked adaptive change, characterized by transient increase and gradual recovery to basal level in c-fos mRNA/c-fos protein (Fos) expression in the hypothalamic paraventricular nucleus (PVN) and in plasma adrenocorticotropin (ACTH) levels, although circulating corticosterone (CORT) remained at a high level. In order to investigate the HPA response to another stressor during the adaptive phase of long-duration RTS, we superimposed acute cold stressor (CS) to 16 hours RTS rats. Superimposed CS-induced re-expression of c-fos mRNA/Fos in the parvocellular region of the PVN (PVNpv) was observed in 16 hours RTS rats. The degree of expression of c-fos gene in superimposed CS rats was the same as those observed in single CS rats. The plasma ACTH levels induced by superimposed CS in 16 hours RTS rats were significantly higher compared with those in single CS rats. On the other hand, there were no significant differences between plasma CORT levels induced by superimposed CS in 16 hours RTS rats and those in single CS rats, and between plasma CORT levels before and after additional CS exposure in 16 hours RTS rats. The present study indicated that c-fos gene expression in PVN induced by superimposed CS was normo-responsive, ACTH secretion was hyper-responsive (facilitation), CORT secretion was slightly increased, but not hyper-responsive in long-duration RTS rats. These findings suggest that stress response induced by superimposed CS during long-duration RTS may occur in a different way at each level of the HPA.
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PMID:Superimposed cold stress-induced hypothalamic-pituitary-adrenal response during long-duration restraint stress. 1250 52

The effects of an acute toxic dose of cocaine (COC) (60 mg/kg, i.p.) as a stressor were examined in rats both neuroendocrinally and behaviorally. The time course (5 min, 5, 12, and 24 h) of the alterations in the immunoreactivity of POMC (preopiomelanocortin)-derived neuropeptides [ACTH (adrenocorticotropin), beta-endorphin, and alpha-MSH (melanocyte stimulating hormone)] and immediate-early gene-derived proteins (c-fos and egr-1 proteins) was examined in the hypothalamus, including the regions reported to be neuroendocrinally sensitive to stressor effects, along with the accompanying alterations in the spontaneous behaviors in the cage and the forced swimming behaviors. Similar to the observations in rats treated with a 30 min immobilization stress (IM), an increase in the number of immunoreactive nerve cells for each neuroendocrinal product and a delayed depression in the swimming behaviors as compared to the alterations in the spontaneous activity, which seemed to be correlated with some intermediate steps, were characteristically caused by a toxic dose of COC. However, the early enhancement (at 5 h) of the swimming behaviors and the brain ACTH level might also be the characteristic acute COC effects, which could be differentiated from the effects of other non-psychostimulant stressors.
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PMID:Increased immunoreactivity of POMC-derived neuropeptides and immediate-early gene-derived proteins (c-Fos and Egr-1 proteins) as an early step of acute cocaine-induced stressor effects: comparison with the effects of immobilization stress. 1260 46

Adrenocorticotropic hormone (ACTH) release from anterior pituitary corticotropes is greatly increased during peripheral inflammation induced by lipopolysaccharide (LPS) administration. Interleukin-6 (IL-6) is thought to participate in LPS-induced ACTH release, but whether or not corticotropes are directly targeted by this cytokine is unclear. Therefore, we investigated the expression and activation of IL-6 signaling components in the pituitary of rats 2 and 4 h after administration of LPS (250 microg/kg). Intraperitoneal LPS treatment provoked the nuclear translocation of signal transducer and activator of transcription 3 (STAT-3) and Fos expression in the anterior pituitary lobe, as demonstrated by immunohistochemistry. By using in situ hybridization, we demonstrated that suppressor of cytokine signaling 3 (SOCS-3) and c-fos mRNAs were significantly induced by the LPS treatment in the anterior lobe of the pituitary. Dual in situ hybridization revealed that most corticotropes expressed IL-6 receptor and gp130 mRNAs, and that 2 h after LPS treatment, SOCS-3 and c-fos mRNAs were induced in corticotropes. Our results suggest that LPS-induced IL-6 could regulate the hypothalamo-pituitary-adrenal axis by directly targeting corticotropes during peripheral inflammation.
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PMID:In vivo activation of the interleukin-6 receptor/gp130 signaling pathway in pituitary corticotropes of lipopolysaccharide-treated rats. 1262 39

The investigational subject of immunophysiology (neuroimmunomodulation, psychoneurophysiology) is known to be the studies of interactions between nervous and immune systems in normal and pathological conditions on different structural levels of interactions between these systems. It has been shown that expression of genes of immediate (c-fos) and rapid (IL-2) reactions in response to stimuli of non-immune nature occurs not only in lymphoid cells, but also in certain structures of central nervous system. In addition, there are many facts, demonstrating the elevation of IL-1 production by cells of monocyte-macrophage system and the expression of IL-1 genes in brain after action of irritants of different origin. The IL-1 level is revealed to be increased after action of different stress factors that can be predictable. The studies are started having concern with rather new and extremely important aspect of immunophysiology, that is the studies of cytokine expression in brain and its role in brain function. Now it is already clear that practically all the spectrum of cytokines is present in brain and many of them, including IL-1 and IL-2, are expressed not only on glial cells, but on neurons. Partly cytokine involvement is shown during the development of regulatory processes. For example, IL-1 and IL-2 stimulate production of corticotropin releasing and lutein stimulating factors. It is possible to suggest that this line of studies would be highly perspective either for immunology, or for physiology of XXI century.
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PMID:Contemporary Topics in Neuroimmunomodulation. 1268 52

There is a growing literature that indicates that exposure to elevated levels of glucocorticoids can result in long term consequences for the developing brain. In the developing rodent there is a period from about day 4-14 when the adrenal response to stress is either minimal or non-existent thus resulting in stable low levels of circulating glucocorticoids. This has been designated as the stress hypo-responsive period (SHRP). Numerous experiments have demonstrated that maternal factors are critical for the regulation of the pup's hypothalamic-pituitarty adrenal (HPA) axis and the maintenance of the SHRP. Following 24 h of maternal deprivation the neonatal rat shows elevated basal levels of corticosterone and exhibits a robust corticosterone and ACTH response to mild stress. Further c-fos mRNA in the paraventricular nucleus is enhanced following stress in deprived pups. At least three aspects of maternal behavior play a role in the regulation of the HPA axis during development. Tactile stimulation appears capable of inhibiting most of the brain-related changes that occur following maternal deprivation. Feeding is essential for maintaining the adrenal unresponsive and reduces the sensitivity of the adrenal to ACTH. Passive contact suppresses the response to stress. In the adult corticotropin-releasing hormone (CRH) is the major neuropeptide that controls pituitary ACTH secretion. In the maternally deprived pup CRH gene transcription is down regulated and arginine vasopressin (AVP) appears to assume the major regulatory hormone that modulates ACTH. These data all indicate that maternal factors are responsible for actively inhibiting the endocrine responses to stress postnatally. Further, maternal deprivation also results in increased cell death in several brain regions. Thus during development most of the peripheral and central stress responsive systems are capable of being activated. However, under conditions of normal dam-pup interactions these responses are mostly suppressed by the dam's behavioral interaction with the pups thus preventing the potential toxic effects of increased secretion of glucocorticoids during critical periods of brain development.
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PMID:Regulation of the hypothalamic-pituitary-adrenal axis in the neonatal rat: the role of maternal behavior. 1275 66

Strong c-fos expression was induced in neuronal cells of several brain nuclei and the auditory cortex by a short duration auditory stimulation (white noise) in rats. By double immunostaining, Fos-immunoreactive cell nuclei appeared in corticotropin-releasing hormone (CRH)-containing neurons in the hypothalamic paraventricular nucleus, but not in CRH neurons elsewhere in the brain including the central nucleus of the amygdala. Among brain catecholaminergic neurons, only cells in the medulla oblongata (in the A1/C1and A2/C2 cell groups) established double immunostaining for Fos and tyrosine hydroxylase. Sound stimulus in rats with unilateral tympanotomy and plugging the airways resulted in side differences of Fos immunoreactivity in neurons of the auditory pathways and the auditory cortex, but the effect was bilateral in hypothalamic and amygdaloid nuclei. The present data provide evidence for the participation of CRH-synthesizing neurons in hypothalamus and medullary catecholaminergic neurons in the central organization of responses to audiogenic stress stimuli.
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PMID:Acute audiogenic stress-induced activation of CRH neurons in the hypothalamic paraventricular nucleus and catecholaminergic neurons in the medulla oblongata. 1276 88

Housing rats in an enriched environment improves functional outcome after ischemic stroke, this may reflect neuronal plasticity in brain regions outside the lesion. Which components of the enriched environment that are of greatest importance for recovery after brain ischemia is uncertain. We have previously found that enriched environment and social interaction alone both improve functional recovery after focal cerebral ischemia, compared with isolated housing with voluntary wheel-running. In this study, the aim was to separate components of the enriched environment and investigate the effects on some potential mediators of improved functional recovery; such as the inducible transcription factors nerve growth factor-induced gene A (NGFI-A) and NGFI-B, and the glucocorticoid and serotonin systems. After permanent middle cerebral artery occlusion, rats were divided into four groups: individually housed with no equipment (deprived group), individually housed with free access to a running wheel (running group), housed together in a large cage with no equipment (social group) or in a large cage furnished with exchangeable bars, chains and other objects (enriched group). mRNA expression of inducible transcription factors, serotonin and glucocorticoid receptors was determined with in situ hybridisation 1 month after cerebral ischemia. Rats housed in enriched or social environments showed significantly higher mRNA expression of NGFI-A and NGFI-B in cortical regions outside the lesion and in the CA1 (cornu ammonis region of the hippocampus), compared with isolated rats with or without a running wheel. NGFI-A and NGFI-B mRNA expression in cortex and in CA1 was significantly correlated to functional outcome. 5-Hydroxytryptamine receptor 1A (5-HT(1A)) mRNA expression and binding, as well as 5-HT(2A) receptor mRNA expression were decreased in the hippocampus (CA4 region) of the running wheel rats. Mineralocorticoid receptor gene expression was increased in the dentate gyrus amongst wheel-running rats. No group differences were found in plasma corticosterone levels or mRNA levels of glucocorticoid receptor, corticotropin-releasing hormone, 5-HT(2C) or c-fos. In conclusion, we have found that social interaction is a major component of the enriched environment regarding the effects on NGFI-A and NGFI-B expression. These transcription factors may be important mediators of improved functional recovery after brain infarctions, induced by environmental enrichment.
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PMID:Effects of postischemic environment on transcription factor and serotonin receptor expression after permanent focal cortical ischemia in rats. 1280 85


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