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

Ether stress or intracerebroventricular (i.c.v.) administration of saline, met-enkephalin, or naltrexone raised plasma corticosterone levels in mice. The response to ether stress was abolished by a preceding ether stress or by pretreatment with i.c.v. saline or naltrexone. However, following i.c.v. met-enkephalin, plasma corticosterone was significantly elevated by ether stress, the effect being blocked by simultaneous injection of met-enkephalin and naltrexone. Met-enkephalin appears to prevent fast-feedback inhibition of the hypothalamus-pituitary-adrenal system.
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PMID:The effect of intracerebroventricular administration of methionine-enkephalin on the stress-induced secretion of corticosterone in mice. 46 66

Our previous studies have shown that stimulation of the anteroventral third ventricle region increases atrial natriuretic peptide (ANP) release, whereas lesions of the anteroventral third ventricle or median eminence block the release of ANP from blood volume expansion, suggesting a critical central nervous system participation in this response. ANP is also produced within neurons that have cell bodies in the rostral hypothalamus and axons that extend to the median eminence and neural lobe. In addition to its natriuretic effect, the peptide can inhibit the release of corticotropin (ACTH) and prolactin, anterior pituitary hormones that are released during stress. To determine the physiologic significance of ANP in the control of basal and stress-induced release of anterior pituitary hormones, highly specific antiserum against the peptide (AB-ANP) was microinjected into the third cerebral ventricle of conscious freely moving male rats to immunoneutralize hypothalamic ANP. In the initial experiment, the antiserum or control normal rabbit serum (NRS) was injected into the third cerebral ventricle to determine the effect of the antiserum on basal release of pituitary hormones. The antiserum had no effect on the concentrations of plasma ACTH, prolactin, or thyroid-stimulating hormone for 3 hr after the injection; however, plasma growth hormone concentration, although unchanged for 2 hr, was markedly elevated at 3 hr. These results indicate that although ANP appears to have no effect on the basal release of the other hormones, it has a physiologically significant inhibitory effect on growth hormone release. The delay of the effect is probably related to the time required for the antiserum to diffuse to the site of action of the peptide, presumably at some distance from the ventricle. Since this effect was demonstrable only after 3 hr, in the stress experiment, the antiserum or NRS was microinjected into the third ventricle 3 hr prior to application of ether stress. The rapid elevation of plasma ACTH in NRS-injected rats was markedly augmented by AB-ANP. Ether also induced a rapid increase in plasma prolactin in the NRS-injected animals, as expected. Contrary to the ACTH response, the maximal increase in plasma prolactin after ether was attenuated in animals preinjected with AB-ANP. In the NRS-injected animals, there was a significant decline in plasma growth hormone after the application of ether that was significantly accentuated by AB-ANP, but this was probably the result of the higher initial levels of plasma growth hormone in the ANP-AB group followed by its disappearance with a half-time similar to that of the NRS-injected group. The decline in plasma thyroid-stimulating hormone after ether stress was unaltered in the animals injected with AB-ANP. The results of these immunoneutralization studies suggest that endogenous ANP does not play a role in thyroid-stimulating hormone release. On the other hand, the endogenous peptide appears to have a physiologically significant inhibitory role in suppressing ACTH release during stress, mediated at least partly by suppression of vasopressin release. Endogenous ANP has a pathophysiologic role in augmenting the prolactin release in stress either by inhibiting release of prolactin-inhibiting factors or, alternatively, by enhancing release of prolactin-releasing factors. Endogenous ANP appears to inhibit resting, without altering stress-induced inhibition of growth hormone release by stimulating somatostatin release and/or inhibiting growth hormone-releasing hormone release or by both actions.
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PMID:The role of endogenous atrial natriuretic peptide in resting and stress-induced release of corticotropin, prolactin, growth hormone, and thyroid-stimulating hormone. 133 8

A sensitive, specific and reproducible radioimmunoassay was developed for the measurement of alpha-melanocyte-stimulating hormone (alpha-MSH) in the blood plasma of rat. The assay method is based on a sensitive antiserum raised against alpha-MSH in rabbit. The serum is highly specific to alpha-MSH; a HPLC study of an extract of rat plasma showed that the immunoreactivity was given by alpha-MSH. The basal level of alpha-MSH, measured after a simple extraction with ethanol, was found to be 168.3 +/- 16.3 pg/ml (mean +/- SEM). Ether and lysine-vasopressin appeared to be potent stimuli for the peripheral release of alpha-MSH.
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PMID:Specific radioimmunoassay of alpha-melanocyte-stimulating hormone in rat plasma. 254 36

Ether and restraint stress-induced peripheral plasma corticotropin releasing hormone (CRH), arginine vasopressin (AVP), oxytocin (OXY) and adrenocorticotropin (ACTH) levels were measured by radioimmunoassays. Plasma CRH, AVP, OXY and ACTH rose to approximately twice the level of control rats 2 min after the onset of a 1-min exposure to ether. Plasma CRH rose further 5 min after the onset of ether stress, while plasma AVP and OXY returned to the baseline levels at 5 min. Plasma CRH, OXY and ACTH showed significant elevation 2 min after the onset of restraint stress, while plasma AVP did not show a significant change. Plasma OXY and ACTH rose further 5 min after the onset of restraint stress, whereas plasma CRH returned to baseline levels. CRH and OXY concentrations in the hypothalamic median eminence decreased 5 min after the onset of ether exposure and restraint, while the AVP concentration did not differ from control levels. The results, including the discrepancy between plasma CRH and ACTH 5 min after stress, suggest that CRH in the peripheral plasma is derived from both hypothalamic and extrahypothalamic tissues. The levels of stress-induced CRH in the peripheral plasma were sufficient to stimulate ACTH release. These results suggest that ether and restraint stress elevate plasma CRH shortly after the onset of the stress, and that this elevation in the plasma CRH level is at least partly responsible for stress-induced ACTH secretion.
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PMID:Effect of acute ether or restraint stress on plasma corticotropin-releasing hormone, vasopressin and oxytocin levels in the rat. 254 72

The hormonal and neurochemical responses to acute ether stress, morphine, and/or naloxone were analyzed in infantile (13-day-old) and prepubertal (36-day-old) male CD rats in an attempt to identify a possible neurochemical correlate(s) for the previously demonstrated requisite maturation of the PRL response to ether stress. Neuronal serotonin (5-HT), norepinephrine (NE), and dopamine (DA) activities were examined in the medial preoptic hypothalamic area (MPOH), medial basal hypothalamic area (MBH), and median eminence (ME). Ether stress increased plasma PRL, ACTH, and beta-endorphin-like immunoreactivity (beta end) as well as NE metabolism in the MPOH and MBH and neuronal 5-HT activity in the MBH, and decreased neuronal DA activity in the ME of prepubertal animals. Ether stress elicited similar changes in infantile animals, with the important exceptions that plasma PRL, neuronal 5-HT activity in the MBH, and neuronal DA synthesis in the ME were not affected at this earlier age. Morphine increased plasma PRL, ACTH, and beta end levels, elevated neuronal NE and 5-HT activities in the MPOH and MBH, and decreased DA synthesis in the ME in both infantile and prepubertal animals. Naloxone administration did not alter basal hormone concentrations or neuronal monoamine activity in any brain area, but did prevent all of the morphine-induced changes as well as the ether stress-induced changes in PRL, MBH neuronal 5-HT activity, and DA synthesis in the ME of prepubertal animals. In addition, naloxone augmented the ether stress-induced increases in ACTH and beta end in prepubertal rats. Indirect stimulation of 5-HT neurons by administration of the amino acid precursor of 5-HT, 5-hydroxytryptophan, resulted in decreased DA synthesis in the ME of infantile animals and increased plasma PRL levels in that age group, indicating that this portion of the neurochemical connection is already present in infantile animals. Furthermore, the 5-hydroxytryptophan-induced increase in PRL was blocked by pretreatment with naloxone. The results demonstrate that both the ether stress- and morphine-induced increases in plasma PRL, but not in ACTH or beta end, are associated with increased neuronal 5-HT activity in the MBH and a decreased neuronal DA activity in the ME, that these are opiate receptor-mediated effects, and that infantile rats apparently lack a functional opiate-5-HT connection, which matures some time between days 13 and 36 postnatally.
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PMID:Maturation of the prolactin and proopiomelanocortin-derived peptide responses to ether stress and morphine: neurochemical analysis. 300 67

Fourteen adult male rats were successfully implanted in their median eminence with a push-pull cannula perfusing an artificial fluid at a rate of 13 microliters/min, to measure the release of corticotropin releasing factor (rCRF-41) under physiological conditions assessed by baseline plasma adrenocorticotropic hormone (ACTH) levels. In the basal conscious free-moving state, rCRF-41 release displayed a fluctuating pattern, with peaks about every 45 min at a mean value of 9.0 +/- 0.7 pg/15 min sample (n = 42) vs a mean trough value of 4.1 +/- 0.3 pg/sample (n = 44). Ether stress was followed by a striking rise in rCRF-41 release which generally lasted about 45 min and reached mean peak values of 54.3 +/- 3.2 pg/15 min sample (n = 7). These data constitute the first direct measurements of basal and stress-induced CRF releases in conscious unrestrained rats.
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PMID:Evidence for basal and stress-induced release of corticotropin releasing factor in the push-pull cannulated median eminence of conscious free-moving rats. 303 54

Ether-laparotomy stress resulted in a dramatic decrease in specific iodine-125-labeled ovine CRF binding ([125I]oCRF) in the pituitary at 6 h after the onset of the stress although it did not affect [125I]oCRF binding in the pituitary at 2 h after the stress. [125I]oCRF binding was unchanged in the frontal cortex after the stress. In contrast, [125I]interleukin-1 (IL-1)alpha binding was significantly increased in the pituitary at 2 h after the stress and tended to be higher than non-stressed levels at 6 h after the stress but was not statistically significant. Ether-laparotomy stress did not affect [125I]IL-1 alpha binding in hippocampus, spleen and testis at any time after the stress. Plasma adrenocorticotropic hormone (ACTH) and corticosterone were increased at 2 h after the stress. These data demonstrate complex interactions between CRF and IL-1 receptors on HPA axis during stress.
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PMID:Reciprocal modulation of corticotropin-releasing factor and interleukin-1 receptors following ether-laparotomy stress in the mouse. 782 96

The corticotropin-releasing hormone (CRH) gene contains a perfect palindromic motif in its promoter region that allows binding of the cyclic adenosine monophosphate response element binding protein, CREB. Since previous studies suggest that the CRH gene can be activated by cyclic adenosine monophosphate, we determined whether stress and feedback inhibition by glucocorticoids in CRH-producing neurons in the hypothalamic paraventricular nucleus could be mediated by changes in the phosphorylation of CREB. Antisera to CREB and phospho-CREB Ser133 (PCREB), the active phosphorylated form of CREB, were used for immunohistochemical studies on rat brain. In nonstressed animals CREB immunostaining was confined to the nucleus of cells ubiquitously throughout the hypothalamus, while PCREB immunostaining was discretely localized in magnocellular neurons and only a few cells in the medial parvocellular subdivision of the paraventricular nucleus. Ether and handling stress markedly increased the number of PCREB-labeled neurons in the parvocellular subdivision. Double immunolabeling with CRH antiserum revealed that the majority of hypophysiotropic CRH neurons in stressed animals expressed PCREB. Following systemic administration of dexamethasone (100 micrograms/day) for 2.5 days, PCREB immunostaining was completely abolished in parvocellular CRH-producing neurons after ether or handling stress. Dexamethasone had no apparent effect on CREB immunostaining. These results demonstrate that glucocorticoids suppress CREB phosphorylation in hypophysiotropic CRH neurons and suggest that prevention of CREB phosphorylation is a possible mechanism for feedback inhibition of CRH biosynthesis by glucocorticoids.
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PMID:Glucocorticoids inhibit stress-induced phosphorylation of CREB in corticotropin-releasing hormone neurons of the hypothalamic paraventricular nucleus. 926 5

Stress mediators, CRF-41 and vasopressin known to be synthesized in, and released from the parvocellular neurosecretory neurons of the hypothalamic paraventricular nucleus (PVN) are essential to release adrenocorticotropin (ACTH) in response to stress. In addition, suckling-induced prolactin (PRL) release also depends on the integrity of the PVN. In the present study, ether stress-induced adrenocorticotrop hormone (ACTH) and prolactin (PRL) release was studied 2, 5 and 42 days after placing lesions in the hypothalamic paraventricular nucleus (PVN) of male rats. Ether-induced ACTH secretion was strongly inhibited 2 and 5 days after lesions whereas 6 weeks later the lesion induced inhibition was fading. In contrast, PVN lesion failed to inhibit ether-induced PRL release at any time studied. The results suggest that contrary to previous suggestions the peptidergic neurons essential for stress-induced PRL release are outside the PVN.
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PMID:Lesioning of the hypothalamic paraventricular nucleus inhibits ether-induced ACTH but not prolactin release. 950 84

The effect of different alpha 2-adrenoreceptor subtype agonists and antagonists on adrenocorticotrop hormone (ACTH) and beta-endorphin release induced by ether stress was examined. Ether inhalation-induced ACTH and beta-endorphin increase was inhibited by i.c.v. administration of 30 micrograms but not 1 and 10 micrograms clonidine (alpha 2-adrenoreceptor agonist). I.c.v. oxymetazoline (alpha 2A-adrenoreceptor agonist; 1-10-30 micrograms) or the alpha 1-agonist methoxamine (100 micrograms/rat) failed to inhibit the stress-induced rise. Pretreatment with the alpha 1/alpha 2B.C-antagonist prazosin (0.5 mg/kg, i.p.) prevented the effect of clonidine on the ether stress, while the alpha 1/alpha 2A-antagonist WB-4101 (0.5 mg/kg, i.p.) was unable to counteract the inhibitory effect of clonidine. Prazosin alone had no effect on the ether-induced plasma ACTH and beta-endorphin elevation. These results suggest that noradrenaline in the central nervous system may inhibit the stress-induced hypothalamo-pituitary-axis and pituitary beta-endorphin activation via alpha 2B.C-adrenoceptor subtypes and prazosin may antagonize its effect on these receptors.
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PMID:Alpha 2-adrenoreceptor subtypes regulate ACTH and beta-endorphin secretions during stress in the rat. 1010 37


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