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 purpose of this study was to investigate the effect of oral administration of progesterone (15 micrograms norethindrone, NE) in presence and absence of estradiol (1 microgram ethinyl estradiol, EE2) on the CNS levels of beta-endorphin like immunoreactivity (beta-EI) in female rats. In acute study (5 days), NE alone did not change beta-EI significantly in pituitary. NE and EE2 together decreased beta-EI by 37% (47% at 10X dose). In chronic study (7 weeks), 2NE had no significant effect on pituitary beta-EI, however, NE and EE2 together at 10X dose decreased it by 14%. In the hypothalamus, NE alone or in presence of EE2 had no significant effect on beta-EI, but 10X dose of NE+ EE2 caused 50 and 76% decrease in beta-EI in acute and chronic study. Striatum was the only tissue where NE alone caused a decrease of 82% in beta-EI when given acutely and 52% when given chronically. EE2 had some protective effect on this decrease since when given together (NE+EE2) the decrease in beta-EI was 21% in acute and 43% in chronic study. Thus our results, along with other studies on the regulation of gonadotropin levels by opioids, suggest that oral contraceptives alter the level of beta-EI and in turn may regulate the release of gonadotropins. Morphine and endogenous opioids have been shown to decrease gonadotropin secretion in various species including humans, apparently by suppressing the release of LH-RH from the hypothalamus (1-5). The opiate antagonist naloxone not only causes up to 10-fold increase in the secretion of gonadotropins (1,3, 6-9) but also opposes the negative feedback effect of steroids on the hypothalamic-pituitary-gonadotropin axis (8), suggesting a regulatory interaction between the endogenous opioids, gonadotropins and gonadal steroids. Like ACTH, the secretion of beta-endorphin is inhibited by glucocorticoids (10). Naloxone induced release of LH is facilitated by estradiol in humans (11) suggesting an antagonistic effect of estradiol on the endogenous opioids. beta-endorphin may play a significant role in neurochemical mechanisms of gonadotropin release in the human menstrual cycle. A preovulatory increase of beta-endorphin in serum occurs 2 days prior to LH surge and a postovulatory decrease in beta-endorphin occurs 5 days later.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effect of oral contraceptives on the rat brain and pituitary beta-endorphin. 631 7

The effect upon steroidogenesis of adding various steroids produced by the placenta was studied in short term cultures of human fetal adrenal cells. The addition of high concentrations (10(3) ng/ml) of estrone or estriol inhibited the production of cortisol, but only the former elicited a parallel increase in dehydroepiandrosterone (DHA) production. Estradiol was effective in inhibiting delta-4-3-ketosteroid production at concentrations of 10-100 ng/ml, levels which approach those found in the fetal circulation, while DHA production was increased at concentrations of 1 microgram/ml. The addition of progesterone (4 microgram/ml) to the medium caused increased production of cortisol and corticosterone, but had no effect on DHA production. Pregnenolone (4 microgram/ml) increased the basal production of DHA and slightly impaired both basal and ACTH-stimulated aldosterone production, but had no effect on cortisol production. The data demonstrate that the many fetal and placental factors which have been studied to date, only ACTH and estrogens can interact to produce the characteristic fetal pattern of steroidogenesis. Preliminary studies indicate that this effect-stimulated aldosterone production, but had no effect on cortisol production. The data demonstrate that the many fetal and placental factors which have been studied to date, only ACTH and estrogens can interact to produce the characteristic fetal pattern of steroidogenesis. Preliminary studies indicate that this effect-stimulated aldosterone production, but had no effect on cortisol production. The data demonstrate that the many fetal and placental factors which have been studied to date, only ACTH and estrogens can interact to produce the characteristic fetal pattern of steroidogenesis. Preliminary studies indicate that this effect of estrogen is not influenced by other peptide hormones such as hCG, human prl, beta-lipotropin, corticotropin-like intermediate lobe peptide, or beta-endorphin. A revised model of the fetoplacental steroidogenic unit is presented which may explain both normal and fetal hyperplasia and postnatal involution of the adrenal cortex and the variations from this pattern seen in apituitary children.
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PMID:The control of steroidogenesis by human fetal adrenal cells in tissue culture. IV. The effect of exposure to placental steroids. 645 37

Different anaesthetic procedures that were used during an in vitro fertilisation and embryo transfer (IVF-ET) program have been analysed in order to determine their influence on plasma levels of estradiol, progesterone, prolactin, and beta-endorphin and results of IVF-ET. METHODS. Fifty-four patients awaiting transvaginal oocyte aspiration were randomised into three groups: (1) anaesthesia with ketamine as an induction agent and analgesic (n = 20); (2) general intubation anaesthesia using thiopentone for induction and enflurane for maintenance (n = 18); and (3) no anaesthesia (n = 16). Estradiol, progesterone, prolactin, and beta-endorphin were measured from day 3 to 14 referring to follicle aspiration. Differences between preoperative hormone levels and their intra- and postoperative peaks were analysed using the Kruskal-Wallis test (P < 0.03). The results were corrected using the Holms method (alpha = 0.05). RESULTS. No differences were observed in estradiol and progesterone levels (Figs. 1, 2). Prolactin levels were 1.4 times higher (P < 0.001) when ketamine was used and 2.2 times higher (P < 0.001) after short general anaesthesia than in the control group (Fig.3). Similar results were observed with respect to beta-endorphin: in comparison with the control group we found significant elevation by a factor of 2.1 when ketamine was used (P < 0.001). The discrepancy became even more marked with general anaesthesia: beta-endorphin was 3.9 times higher compared to the controls (P < 0.001) (Fig.4). Comparing the two groups who were given anaesthetics, prolactin and beta-endorphin levels were also significantly different (P < 0.001). The IVF procedure itself did not appear to be affected by different anaesthetic procedures during oocyte aspiration (Table 2). CONCLUSIONS. The increased prolactin and beta-endorphin plasma levels associated with ketamine and general anaesthesia reflect a significant alteration of the observed hormone levels. When anaesthesia is indicated, we try to avoid general intubation anaesthesia in favor of ketamine.
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PMID:[The effect of different anesthetic procedures on hormone levels in women. Studies during an in vitro fertilization-embryo transfer (IVF-ET) program]. 867 85

The present investigation was conducted to evaluate the effects of estradiol and progesterone on beta-endorphin and Met-enkephalin levels in specific brain regions of ovariectomized rats. Female Sprague-Dawley rats (100-120 g) adapted to a 12-hour light, 12-hour dark illumination cycle were used in these studies. Animals were ovariectomized under pentobarbital anesthesia. After a recovery period of 10-14 days, estradiol (50 micrograms/kg in 0.2 ml olive oil) was administered subcutaneously to rats at either 8.00, 14.00 or 16.00 h, progesterone (5 mg/kg in 0.1 ml olive oil) or estradiol plus progesterone was administered subcutaneously at 16.00 h. Control rats were injected with olive oil. Animals were sacrificed 2 h later. The cerebral cortex, hypothalamus, hippocampus and midbrain were dissected, and their beta-endorphin and Met-enkephalin levels were determined by radioimmunoassay. Estradiol administration at 8.00 h resulted in a significant decline in beta-endorphin levels of the hippocampus (66% decrease) and a significant rise in Met-enkephalin levels of the hypothalamus (37.8% increase) but had no effect on other brain regions studied. When estradiol was administered at 14.00 h, it produced a significant change in beta-endorphin levels in the cerebral cortex (34.7% increase) and in the midbrain (31.3% increase), but these levels were not altered in the other brain regions. At 16.00 h estradiol and progesterone alone caused a significant increase (29 and 43%, respectively) in beta-endorphin levels of the hippocampus. Similarly, the Met-enkephalin levels in the hippocampus significantly increased following administration of estradiol (57% increase) and progesterone (54% increase) alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diurnal variation in the acute effects of estradiol and progesterone on beta-endorphin and Met-enkephalin levels in specific brain regions of ovariectomized rats. 797 34

Estradiol provides physiological signals to the brain throughout life that are indispensable for the development and regulation of reproductive function. In addition to its multiple physiological actions, we have shown that estradiol is also selectively cytotoxic to beta-endorphin neurons in the hypothalamic arcuate nucleus. The mechanism underlying this neurotoxic action appears to involve the conversion of estradiol to catechol estrogen and subsequent oxidation to o-semiquinone free radicals. The estradiol-induced loss of beta-endorphin neurons engenders a compensatory increment in mu opioid binding in the medial preoptic area rendering this region supersensitive to residual beta-endorphin or to other endogenous opioids. The consequent persistent opioid inhibition results in a cascade of neuroendocrine deficits that are ultimately expressed as a chronically attenuated plasma LH pattern to which the ovaries respond by becoming anovulatory and polycystic. This neurotoxic action of estradiol may contribute to a number of reproductive disorders in humans and in animals in which aberrant hypothalamic function is a major component.
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PMID:Pathologic effect of estradiol on the hypothalamus. 821 28

The density of beta-endorphin (beta-endo)-like immunoreactive (IR) fibers in the medial preoptic area (MPOA) has been shown to vary across the estrous cycle and is gonadal steroid hormone-dependent. These beta-endo-containing fibers are presumably projections of proopiomelanocortin (POMC) neurons which are located in the arcuate nucleus (ARC). POMC mRNA level varies across the estrous cycle in the ARC and its expression is differentially altered by gonadal steroid hormones. However, it is unclear how gonadal steroids regulate POMC gene expression in ARC neurons that innervate the MPOA. Therefore, combined fluorogold (FG) retrograde neuronal labeling and in situ hybridization histochemistry were used to investigate the effects of gonadal steroid hormone treatment on POMC gene expression in ARC neurons supplying the MPOA of ovariectomized (OVX) female rats. POMC-expressing cells were located in the ARC and median eminence (ME), wherein such neurons were significantly larger than unlabeled cells that surround them. A relatively greater number of ARC POMC neurons were observed to innervate the medial portion of the medial preoptic nucleus (MPN) than the lateral portion of the MPN. Estradiol (E2) and progesterone (P) treatment before FG injection did not affect the number of FG and POMC double-labeled neurons in the ARC, which suggests that hormone treatment did not alter the number of POMC-expressing neurons projecting to the MPN. In OVX animals, ARC POMC mRNA labeling was relatively low, and increased significantly in neurons of the most rostral ARC region 48 h after E2 treatment. P administration enhanced and prolonged the effect of E2 in this group of ARC neurons. E2P treatment significantly increased POMC mRNA expression beginning 13 h after P injection in all but the most caudal ARC POMC neurons. Thereafter, E2P treatment gradually increased POMC mRNA expression for at least 1 additional day. Gonadal steroid hormone treatment apparently affects POMC mRNA expression uniformly in neurons of the same ARC subdivision without regard to their efferent targets. Diurnal variation of POMC mRNA expression is present only in the most rostral ARC region, which contains a population of E2-sensitive POMC neurons. The results suggest that the relatively greater beta-endo-like IR fiber density in the medial MPN is due to a greater number of POMC neurons innervating this region. The pattern of innervation of the MPN by POMC neurons is unaffected by gonadal steroid hormone treatment, which appears to induce POMC expression in ARC neurons, and eventually to stimulate the synthesis and transport of beta-endo in POMC neuronal axons which project to the MPOA.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Gonadal steroid hormone regulation of proopiomelanocortin gene expression in arcuate neurons that innervate the medial preoptic area of the rat. 853 66

Parturition in sheep is initiated by increases in activity of the fetal hypothalamic-pituitary-adrenal axis. We have previously reported that cortisol negative feedback efficacy is decreased at the end of gestation. The present study was designed to test the hypothesis that increasing plasma estrogen and/or androgen concentrations in the fetus might increase plasma adrenocorticotropic hormone (ACTH) concentration, either by stimulating ACTH secretion or by altering the negative feedback effect of cortisol on ACTH. Fetal sheep were chronically catheterized and treated with no steroid (control), 17beta-estradiol, or androstenedione (each approximately 0.24 mg/day). After catheterization and implantation of steroid pellet, fetuses were subjected to two short (10 min) periods of sodium nitroprusside-induced hypotension with or without pretreatment with intravenous infusion of hydrocortisone sodium succinate (0.5 microg/min) to test fetal ACTH responsiveness to stress and cortisol negative feedback efficacy. Estradiol treatment significantly increased basal plasma ACTH and cortisol concentrations relative to control fetuses but did not interfere with the inhibition of ACTH secretion by cortisol. Fetal plasma ACTH responses to hypotension were significantly suppressed approximately 60% in both control and estradiol-treated groups. Androstenedione treatment significantly increased basal fetal plasma ACTH and decreased basal fetal plasma cortisol concentration. Androstenedione did not alter stimulated levels of fetal ACTH but did block the inhibition of stimulated ACTH by cortisol. We conclude that increased fetal cortisol and ACTH secretion at the end of gestation may be due to the combined effects of the gonadal steroids in that estradiol increases basal plasma ACTH secretion while androstenedione reduces cortisol negative feedback efficacy.
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PMID:Modulation of ovine fetal adrenocorticotropin secretion by androstenedione and 17beta-estradiol. 914 11

Of heuristic value in understanding the neurochemistry of major depression is whether the hypothalamo-pituitary-adrenocortical (HPA) axis hyperactivity that occurs in this illness can be related to putative neurotransmitter dysfunction(s). Cholinergic neurotransmission stimulates hypothalamic corticotropin releasing hormone (CRH) and arginine vasopressin (AVP) secretion, both of which stimulate pituitary corticotropin (ACTH) secretion, but whether the HPA axis in humans is activated only by doses of cholinergic agonists that produce noxious side effects remains controversial. To test the hypothesis of increased cholinergic sensitivity in major depression, physostigmine (PHYSO), a reversible cholinesterase inhibitor, was administered to patients and control subjects at a dose that elevated plasma ACTH, cortisol, and AVP concentrations but produced few or no side effects. Exogenous AVP also was administered to determine if it would augment the effect of low-dose PHYSO on the HPA axis. Twelve premenopausal or estrogen-replaced female major depressives, 12 individually matched female control subjects, eight male major depressives, and eight matched male control subjects underwent four test sessions 5-7 days apart: PHYSO (8 microg/kg IV), AVP (0.08 U/kg IM), PHYSO + AVP, and saline control. Serial blood samples were taken before and after pharmacologic challenge and analyzed for ACTH1-39, cortisol, and AVP. Estradiol and testosterone were also measured at each test session. PHYSO (8 microg/kg) significantly increased plasma ACTH, cortisol, and AVP, while producing no side effects in approximately half the subjects and predominantly mild side effects in the other half. These hormone increases following PHYSO occurred primarily in the female depressives and the male control subjects and were not significantly related to the presence or absence of side effects. The greater the ACTH and AVP responses to PHYSO, the stronger their correlation, suggesting that AVP may have been acting as a secretagogue for ACTH. Administered AVP significantly increased the secretion of ACTH in the patients and control subjects to a similar degree, and AVP given after PHYSO did not augment the HPA axis response to a greater degree in the depressives than in the control subjects. Plasma estradiol and testosterone were within the normal range for all four groups of subjects and were not significantly related to their HPA axis hormone responses. The study results support the hypothesis of heightened cholinergic sensitivity in premenopausal female, but not in male, patients with major depression. The low dose of PHYSO used may represent a useful paradigm for central cholinergic stimulation of the HPA axis.
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PMID:Hypothalamo-pituitary-adrenal cortical responses to low-dose physostigmine and arginine vasopressin administration: sex differences between major depressives and matched control subjects. 1064 73

Estradiol, progesterone and some of their metabolites modulate the activity of neurotransmitters and neuropeptides in the CNS. The distribution and concentrations of sex steroids in the various CNS regions is partly dependent on the serum levels, but also on the local synthesis of the steroids. In general, estradiol and testosterone exert a stimulatory, progesterone an inhibitory effect on neuronal activities which are mediated by excitatory (e.g. glutamate, aspartate), and inhibitory amino acids (e.g. GABA) and neuropeptides (e.g. beta-endorphin), respectively. Gonadotropin release is primarily governed by the rhythm of pulsatile secretion of GnRH in the hypothalamus which is controlled by estradiol and progesterone by means of inhibitory or stimulatory modulation of the amplitude and frequency of GnRH pulses. The discharges of GnRH neurons triggered by excitatory amino acids are modulated by estradiol, while the inhibitory effect of progesterone is mediated by GABA and beta-endorphin which cause hyperpolarization of the GnRH neurons and consequently a reduced pulse frequency. The pulse amplitudes are primarily influenced by estradiol, but neuropeptide Y, neurotensin and noradrenaline contribute to their preovulatory enhancement. The postovulatory rise in core temperature is caused by the increasing level of progesterone and its metabolite 3 alpha-pregnanolone, respectively. Despite of this, up to 20% of ovulatory cycles do not show any rise in body temperature. Although 3 alpha-pregnanolone has sedative activities, there is no change in sleep quality during the luteal phase due to their low serum levels. It could be demonstrated that performance on tests of articulatory and fine motor skills are enhanced in the late follicular phase as compared to the menstruation phase, while spatial ability was better during menses. Estrogens may influence mood and well-being in a favorable manner, while in predisposed women progesterone may cause symptoms of premenstrual syndrome. In most women there are, however, no cycle-dependent mood changes. An increase in appetite can be observed during the periovulatory phase and before menses, while sexual interest increases in the follicular phase. Somatic complaints (back pain, abdominal pain, breast tenderness) which are highest before and during menstruation, are probably associated with a lowered pain threshold due to a fall in the beta-endorphin levels in the CNS.
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PMID:[Influence of the ovarian cycle on the central nervous system]. 1201 35

The present study investigated the effects of long-term estradiol withdrawal (ovariectomy) on hypothalamic serotonin-1A (5-HT(1A)) receptor signaling. Changes in neuroendocrine responses to the 5-HT(1A) agonist 8-OH-DPAT and levels of G(z) protein in the hypothalamus were used to examine 5-HT(1A) receptor signaling. Five days following ovariectomy, rats received daily injections of either 2 microg of beta-estradiol 3-benzoate or vehicle (subcutaneously) for 2, 4 or 14 days. Twenty-four hours after the last injection, and 15 min prior to sacrifice, rats were injected with (+/-)8-OH-DPAT (50 micro;g/kg, s.c.) or saline. Estradiol treatment did not alter basal corticotropin (ACTH) or oxytocin levels. Injection of (+/-)8-OH-DPAT produced significant increases in plasma ACTH and oxytocin levels. In the vehicle-treated rats, hormone responses to 8-OH-DPAT were enhanced in rats that received injections for 14 days compared with rats that received injections for either 2 or 4 days. Estradiol treatment for 4 or 14 days blunted this enhanced ACTH response to 8-OH-DPAT, whereas the oxytocin response to 8-OH-DPAT was only blunted after 14 daily injections of beta-estradiol 3-benzoate. The treatment with beta-estradiol 3-benzoate (2 microg/rat) did not reduce membrane-associated G(z) protein levels in the paraventricular nucleus of the hypothalamus. Hence, the inhibitory influence of a low dose of beta-estradiol 3-benzoate on 5-HT(1A) receptor signaling in the hypothalamus is not accompanied by a change in the levels of G(z) protein in the paraventricular hypothalamic nucleus. Results from the present study indicate a supersensitivity of 5-HT(1A) receptors after withdrawal of estradiol and suggest that estradiol suppresses 5-HT(1A) receptor signaling.
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PMID:Ovariectomy-induced increases in hypothalamic serotonin-1A receptor function in rats are prevented by estradiol. 1256 42

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