UNIPROT:P01178 - FACTA Search

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Query: UNIPROT:P01178 (oxytocin)
15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The bed nuclei of the stria terminalis (BNST) is a target site for the central actions of oxytocin (OT) in promoting behavioural and neuroendocrine responses involved in female reproduction, and binding studies suggest that OT sensitivity may be modulated over the peripartum period. Electrophysiological recordings from brain slices in vitro showed that OT sensitivity of BNST neurones is relatively low in late pregnancy, but is high during lactation. In vivo studies over the immediate peri-partum period revealed that although BNST neurones can be excited by i.c.v. OT at day 22 of pregnancy, there is a 5-10 min delay in their response which is not present in lactation. This delay can be reversed by naltrexone, or lesioning the stria terminalis, and may involve an inhibitory opioid input to the BNST from the amygdala. Examination of the role of steroids in regulating OT responses of BNST neurones showed that oestradiol pre-treatment in late pregnant ovariectomized rats increased OT excitation of BNST neurones in vitro, and a similar result was observed with in vivo recordings. Progesterone also augmented OT excitation of BNST neurones in vitro, but no such effect was observed in vivo. This difference could indicate that an additional effect of progesterone is to potentiate extraneous inhibitory inputs to the BNST, or may reflect the ability of this steroid to suppress OT sensitivity by a direct membrane action. Changes in the response of BNST neurones to OT may have functional implications for the action of central OT in facilitating the neuroendocrine milk-ejection reflex (i.e. increasing milk-ejection frequency), an effect which first appears at around day 3 of lactation. Studies involving steroid treatment of late pregnant ovariectomized rats showed that this facilitatory mechanism can be induced to appear early (i.e. on day 22 of pregnancy) by oestradiol, but not progesterone treatment. Collectively, these results support this view, that the action of OT in the BNST is regulated by the changing levels of steroids towards the end of pregnancy, thereby ensuring appropriate neuroendocrine responses necessary for motherhood.
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PMID:Electrophysiological effects of oxytocin within the bed nuclei of the stria terminalis: influence of reproductive stage and ovarian steroids. 1007 97

Estrogen receptor alpha (ERalpha) and estrogen receptor beta (ERbeta) are differentially distributed in the brain and likely mediate different estrogen-dependent processes. ERbeta is abundant in the bed nucleus of the stria terminalis, medial preoptic nucleus, paraventricular nucleus of the hypothalamus and the amygdala of the rat. In the paraventricular nucleus, which is devoid of ERalpha, ERbeta is colocalized with the neuropeptides, oxytocin and vasopressin, suggesting a potential functional role for ERbeta in the regulation of these peptides. We examined the regulation of ERbeta mRNA expression in the rat brain by 17beta-estradiol and the phytoestrogen, coumestrol. 17beta-Estradiol treatment decreased ERbeta mRNA in situ hybridization signal by 44.5% in the paraventricular nucleus of the hypothalamus (PVN), but had no effect in the bed nucleus of the stria terminalis (BnST) or the medial preoptic nucleus (MPA). In contrast, dietary exposure to coumestrol increased ERbeta mRNA signal by 47.5% in the PVN but had no effect in the BnST or the MPA. These data demonstrate that like ERalpha, ERbeta is down regulated by estrogen in a region specific manner in the rat brain. Furthermore, exposure to coumestrol may modulate ERbeta-dependent processes by acting as an anti-estrogen at ERbeta. This data contradicts results from cell transfection assays which suggest an estrogenic activity of coumestrol on ERbeta, indicating that the mode of action may be tissue specific, or that metabolism of dietary coumestrol may alter its effects. Because the highest concentrations of phytoestrogens are found in legumes, vegetables and grains, they are most prevalent in vegetarian and traditional Asian diets. Understanding the neuroendocrine effects of phytoestrogens is particularly important now that they are being marketed as a natural alternative to estrogen replacement therapy and sold in highly concentrated pills and powders.
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PMID:Regulation of estrogen receptor beta mRNA in the brain: opposite effects of 17beta-estradiol and the phytoestrogen, coumestrol. 1010 Dec 43

The objective of the present study was to further elucidate our previous observation that beta2-adrenoceptor activation induces oxytocin receptor (OTR) expression in rat myometrium. We wanted to investigate whether the mechanism behind this effect was under the influence of gonadal steroids. Ovariectomized non-pregnant rats were treated with estrogen, progesterone or a combination of both for 3 days. Some rats were concomitantly treated with isoproterenol. Estrogen treatment increased both OTR mRNA production and maximal binding of [3H]-oxytocin to isolated myometrial plasma membranes, but it did not affect contractility of isolated uterine strips challenged with oxytocin. When the estrogen regimen was combined with isoproterenol treatment, an augmented maximal contractile response (Emax) to oxytocin was observed although no further increase in OTR mRNA and binding was seen. Progesterone treatment did not in itself alter OTR mRNA, OTR binding or Emax. However, OTRs were induced at the level of gene expression when progesterone was supplemented with isoproterenol infusion. Finally, progesterone suppressed the effect of estrogen on OTR mRNA production and binding when the two compounds were administered together. However, when isoproterenol treatment was added this effect was abolished and Emax was enhanced more than that seen following treatment with estrogen alone. These data suggest that beta2-adrenoceptor activation represents an important regulator of OTR expression/function in estrogen- and progesterone-dominated rat myometrium.
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PMID:Up-regulation of oxytocin receptors in non-pregnant rat myometrium by isoproterenol: effects of steroids. 1033 43

Experiments were undertaken to examine the role of ovarian steroids in peripartum programming of oxytocin sensitivity of limbic neurons implicated in oxytocin-induced facilitation of the milk-ejection reflex. In vivo recordings of neurons in the bed nuclei of the stria terminalis and ventrolateral septum of pre-parturient rats which had undergone prior ovariectomy and hysterectomy showed that oestradiol significantly increased the excitatory responses of bed nuclei/ventrolateral septum neurons to intracerebroventricular oxytocin, compared to oil-treated controls. Oestradiol also increased the excitation of bed nuclei neurons to the selective oxytocin agonist, [Thr4,Gly7]oxytocin in brain slices from steroid pre-treated ovariectomized hysterectomized rats, so that both the proportion of responsive neurons, and the magnitude of their responses were significantly increased. Parallel autoradiographic studies showed that oxytocin binding in the medial bed nuclei and ventrolateral septum was selectively increased following oestradiol treatment. Progesterone pre-treatment had no effect on either oxytocin sensitivity of bed nuclei/ventrolateral septum neurons recorded in vivo, or on oxytocin binding in the medial bed nuclei and ventrolateral septum, compared to oil-treated controls. Mean responses to [Thr4,Gly7]oxytocin in bed nuclei neurons recorded in slices from progesterone-treated rats were larger than controls, but this effect was highly variable. These results demonstrate that oestradiol greatly enhances oxytocin receptor expression and sensitivity of bed nuclei/ventrolateral septum neurons to oxytocin over the peripartum period, consistent with involvement of this steroid in enhancing oxytocin regulation of neuroendocrine and behavioural adaptations required for lactation.
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PMID:Effect of gonadal steroids on the oxytocin-induced excitation of neurons in the bed nuclei of the stria terminalis at parturition in the rat. 1039 88

Progesterone, produced by the ovaries and adrenal glands, regulates reproductive behavior and the surge of luteinizing hormone which precedes ovulation by acting on neurons located in different parts of the hypothalamus. The study of the activation of these reproductive functions in female rats has allowed to explore the different mechanisms of progesterone action in the brain. It has allowed to demonstrate that new actions of the hormone, which have been observed in particular in vitro systems, are also operational in vivo, and may thus be biologically relevant. This mainly concerns the direct actions of progesterone on receptors of neurotransmitters such as oxytocin and GABA. Activation of the progesterone receptor in the absence of ligand by phosphorylation may also play a role.
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PMID:Genomic and membrane actions of progesterone: implications for reproductive physiology and behavior. 1055 89

The role of luteal oxytocin in the generation of luteolytic episodes of prostaglandin F2alpha at luteolysis was investigated. On day 10 of the cycle Dorset ewes underwent either surgical removal of the corpora lutea (lutectomy; n = 4) or sham operation (sham; n = 4). Lutectomised ewes were then administered progesterone by twice daily i.m. injection in corn oil (20 mg/day) until day 14 when treatment was ceased to simulate luteolysis. The concentration of 13, 14 dihydro-15-keto prostaglandin F2alpha (PGFM) was measured in peripheral blood samples collected at 20-min intervals for 8 h on days 12-16 of the cycle. Progesterone and oestradiol concentrations were similar in the two groups over the whole experimental cycle while oxytocin fell dramatically following lutectomy. No prostaglandin F2alpha release episodes were seen on day 12 or 13, while from days 14-16 both groups exhibited a similar episode frequency (lutectomy 0.9/ewe/8 h; sham 0.8/ewe/8 h). Analysis of episode characteristics revealed lower episode amplitude (p<0.05) but longer episode duration (p<0.05) in the lutectomy group. The results demonstrate that a normal frequency of prostaglandin F2alpha release episodes occurs independently of luteal oxytocin secretion. However, luteal oxytocin is involved in regulating the pattern of release, perhaps causing the release of episodes of the magnitude required for the successful completion of luteolysis.
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PMID:The role of luteal oxytocin in episodic secretion of prostaglandin F2alpha at luteolysis in the ewe. 1061 36

Administration of sequential estradiol (E(2)) and progesterone (P) for 2 weeks followed by withdrawal of P 48 h prior to sacrifice will increase oxytocin (OT) messenger ribonucleic acid (mRNA) levels in the paraventricular and supraoptic nuclei (PVN and SON) of the ovariectomized rat. Progesterone is known to mediate certain of its effects via binding to the gamma aminobutyric acid A (GABA(A)) receptor. E(2) and P are known to modulate the specific binding of the GABA(A) receptor agonist, muscimol, in certain brain regions. In the present study ovariectomized rats received empty or steroid-filled Silastic capsules for 2 weeks according to one of the following schedules: E(2) only (E(2) group) vs. sequential E(2) and P in which P was either removed 48 h prior to killing (E(2)/P- group) or sustained until sacrifice (E(2)/P+ group). [3H]muscimol binding was measured in several brain regions of the animals. The steroid sequence that is known to increase SON OT mRNA (E(2)/P-) selectively decreased [3H]muscimol binding in the SON of ovariectomized rats. The results suggest that changes in GABA(A) receptor binding may, in part, play a role in the regulation of steroid-induced increases in hypothalamic OT expression.
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PMID:An ovarian steroid hormone regimen that increases hypothalamic oxytocin expression alters [3H] muscimol binding in the hypothalamic supraoptic nucleus of the female rat. 1070 May 77

This experiment tested the hypothesis that opioid antagonists could influence the timing of the onset and progress of parturition in the pig. Primiparous pigs (gilts) received a jugular catheter on Days 104 to 106 of pregnancy. At 1400 h on Day 112 the gilts received 10 mg PGF2alpha, i.m. to induce parturition. At 1000 h on Day 113 (i.e., 20 h later) gilts received either saline (n=6), 1 mg/kg, i.v. naltrexone (n=4) or 1 mg/kg, i.v. naloxone (n=5). Blood samples were taken daily from Days 108 to 116. On Day 113, blood samples were taken hourly from 0500 to 0900 h and then every 30 min until 2400 h, or until the birth of the last piglet (BLP) (whichever was sooner) and assayed for progesterone, oxytocin (OT), cortisol and PRL. Additional blood samples for OT and cortisol assay were taken every minute from 0930 to 1100 h on Day 113 and for 30 min during parturition. Naloxone, but not naltrexone, delayed the onset of parturition relative to saline controls (by 14 h 21 min; P<0.05). Duration of parturition and rate of births were not significantly affected by treatment. Mean plasma OT increased in the 4 h following naloxone but not saline treatment, during which time OT plasma pulse amplitude was reduced in naloxone and naltrexone-treated animals relative to saline treated controls. The PRL secretion rose following treatment in saline treated animals, consistent with approaching parturition, but failed to rise in opioid antagonist treated animals. Progesterone concentrations remained elevated in naloxone-treated animals for longer than in the other groups. These data suggest that a rapid change in overall effect of parenteral administration of naloxone to parturient pigs occurs from delaying its onset when administered as in these experiments, to facilitating its progress when given during parturition (earlier experiments). The delay of onset of parturition may be mediated by interference with hypothalamic control of OT or PRL release.
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PMID:The timing of parturition in the pig is altered by intravenous naloxone. 1073 Sep 79

Parturition is driven by a pulsatile pattern of oxytocin secretion, resulting from burst firing activity of supraoptic oxytocin neurones and reflected by induction of Fos expression. Rats were injected with progesterone on day 20 of pregnancy to investigate the role of the decreasing progesterone:ratio oestrogen ratio, which precedes delivery, in the activation of supraoptic neurones. Progesterone delayed the onset of birth by 28 h compared with vehicle (control) and prolonged the duration of delivery, which was overcome by pulsatile injections of oxytocin, indicating that the slow delivery may reflect impaired oxytocin secretion. Parturient rats pretreated with progesterone had fewer Fos immunoreactive nuclei in the supraoptic nucleus than did parturient rats pretreated with vehicle. The number of Fos immunoreactive nuclei was not restored after oxytocin injection, indicating that appropriate activation of oxytocin neurones is impaired by progesterone and also that there is a lack of stimulatory afferent drive. Fos expression increased in the nucleus of the tractus solitarius during parturition in rats pretreated with either vehicle or progesterone, but not in rats that had been pretreated with progesterone and induced with oxytocin, indicating that this input was inhibited. Endogenous opioids inhibit oxytocin neurones in late pregnancy and the opioid antagonist, naloxone, increases Fos expression in supraoptic nuclei by preventing inhibition. However, progesterone attenuated naloxone-induced Fos expression in the supraoptic nucleus in late pregnancy and naloxone administered during parturition did not accelerate the duration of births delayed by progesterone administration, indicating that progesterone does not act by hyperactivation of endogenous opioid tone. RU486, a progesterone receptor antagonist, enhanced supraoptic neurone Fos expression in late pregnancy, indicating progesterone receptor-mediated actions. Thus, progesterone withdrawal is necessary for appropriate activation of supraoptic and tractus solitarius neurones during parturition.
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PMID:Effect of progesterone on the activation of neurones of the supraoptic nucleus during parturition. 1105 52

The amount of beta-endorphin-like immunoreactivity (beta-END-LI) in porcine corpora lutea from several stages of the oestrous cycle and the effects of progesterone, oxytocin, and prolactin on beta-END-LI secretion in vitro by luteal cells were studied. Porcine corpora lutea obtained on days 1-5, 6-10, 11-13, 14-18, and 19-21 of the cycle were used to prepare extracts for beta-END-LI determination. Additionally, corpora lutea from days 11-13 and 14-18 were enzymatically dissociated and isolated luteal cells were used for further study of beta-endorphin secretion in vitro. Cells were cultured in serum-free defined M 199 medium (106 cells/ml) at 37 degrees C under 5% CO2 in air, for 12 h. The influences of the following factors on beta-END-LI secretion by luteal cells were tested: progesterone (10-9, 10-7 and 10-5 M), oxytocin (0.01, 0.1, 1 and 10 ng/ml), and prolactin (0.1, 1, 10 and 100 ng/ml). The beta-END-LI contents in extracts and media were measured by radioimmunoassay. The tissue concentration of beta-END-LI was lowest on days 1-5 of the cycle (0.35 +/- 0.03 ng/g wet tissue). Subsequently, it constantly increased to the highest value on days 14-18 (16.58 +/- 0.52 ng/g wet tissue) and on days 19-21 it declined (11.10 +/- 0.52 ng/g wet tissue). Progesterone at a low dose (10-9 M) resulted in significant (p < 0.05) increases and decreases in beta-END-LI secretion by luteal cells from days 11-13 and 14-18, respectively. Higher doses of progesterone (10-7 and 10-5 M) had no effect on beta-END-LI release, compared with the control group. All dose-levels of oxytocin used decreased beta-END-LI secretion by luteal cells on days 11-13 and 14-18 of the cycle. Prolactin at doses of 0.1 and 1 ng/ml on days 11-13, and all doses tested on days 14-18 resulted in decreases in beta-END-LI release from luteal cells. These results document evident changes in beta-END-LI content in the pig corpus luteum during its development and indicate the potential roles of progesterone, oxytocin, and prolactin in luteal cell secretion of beta-END-LI.
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PMID:The content of beta-endorphin-like immunoreactivity in porcine corpus luteum and the potential roles of progesterone, oxytocin and prolactin in the regulation of beta-endorphin release from luteal cells in vitro. 1132 64

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