Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of oxytocin (OT) on growth hormone (GH) secretion was investigated using dispersed rat anterior pituitary cells. OT dose-dependently inhibited GH secretion as well as GHRH-stimulated GH release. The inhibitory actions of OT on GH release were totally abolished by pretreatment with the OT-antagonist VAP 259. The peptides galanin and cholecystokinin did not affect the OT-induced inhibition on basal or GHRH-stimulated GH release. Several possible mechanisms by which OT may influence GH release are discussed.
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PMID:Effect of oxytocin on growth hormone release in vitro. 895 75

The mouse Mf3 gene, also known as Fkh5 and HFH-e5.1, encodes a winged helix/forkhead transcription factor. In the early embryo, transcripts for Mf3 are restricted to the presomitic mesoderm and anterior neurectoderm and mesoderm. By 9.5 days post coitum, expression in the nervous system is predominantly in the diencephalon, midbrain and neural tube. After midgestation, the highest level of mRNA is in the mammillary bodies, the posterior-most part of the hypothalamus. Mice homozygous for a deletion of the mf3 locus on a [129 x Black Swiss] background display variable phenotypes consistent with a requirement for the gene at several stages of embryonic and postnatal development. Approximately six percent of the mf3-/- embryos show an open neural tube in the diencephalon and midbrain region, and another five percent show a severe reduction of the posterior body axis; both these classes of affected embryos die in utero. Surviving homozygotes have an apparently normal phenotype at birth. Postnatally, however, mf3-/- pups are severely growth retarded and approximately one third die before weaning. This growth defect is not a direct result of lack of circulating growth hormone or thyrotropin. Mice that survive to weaning are healthy, but they show an abnormal clasping of the hindfeet when suspended by the tail. Although much smaller than normal, the mice are fertile. However, mf3-/- females cannot eject their milk supply to feed their pups. This nursing defect can be corrected with interperitoneal injections of oxytocin. These results provide evidence that Mf3 is required for normal hypothalamus development and suggest that Mf3 may play a role in postnatal growth and lactation.
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PMID:The winged helix gene, Mf3, is required for normal development of the diencephalon and midbrain, postnatal growth and the milk-ejection reflex. 911 97

The aim of the present study was to investigate the role of oxytocin (Oxy) in the control of growth hormone (GH) release. Oxy was administered subcutaneously (s.c.) or intracerebroventricularly (i.c.v.) to male rats. The animals were decapitated and trunk blood was collected at 30 and 120 min after Oxy administration. GH levels were analyzed by radioimmunoassay. Oxy (100 microg, s.c) increased plasma levels of GH significantly 30 min after administration. Oxy (2 ng, i.c.v.) caused a significant rise of GH after 120 min. This effect was completely abolished by previous administration of the Oxy antagonist 1-deamino-2-D-Tyr-(OEt)-4-Thr-8-Orn-oxytocin. When 5 microg of Oxy were given i.c.v. or 1 mg s.c., an inhibition of GH secretion was seen after 120 min. This effect was also abolished by the Oxy antagonist. Thus Oxy may influence GH in opposite directions depending on the doses given.
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PMID:Evidence for a dual function of oxytocin in the control of growth hormone secretion in rats. 916 76

Restricted feed (RF) and methscopolamine bromide (MB), an anticholinergic agent reported to block growth hormone secretion, were evaluated as potential means for reducing milk production in ewes at weaning. On d 58 +/- 1 postpartum (d 0), 40 fall-lambing ewes were allotted to treatments in a 2 (RF vs full feed [FF]) x 2 (MB vs saline [SAL]) factorial arrangement according to breed, age, and number of lambs born and suckled. On d 0 at 0800, ewes were separated from lambs, injected with 40 IU of oxytocin, and machine milked 30 s later. Ewes remained separated from lambs for 3 h, and at 1100 they were milked and yields were determined. From d 0 through 6, FF ewes received a daily ration of 1.8 kg of alfalfa hay and .9 kg of corn; RF ewes received only 1.8 kg of alfalfa hay. On d 7 at 0800 and 1400, ewes were separated from lambs, milked, treated with a s.c. injection of either 96 mg of MB dissolved in 2 mL of SA or SA alone, and after 3-h separations were milked at 1100 and 1700 and yields determined. Lambs were weaned at 1400. After milking at 1700, all ewes were placed in drylot without feed or water. At 1100 on d 9, residual milk yields were collected. Milk samples were retained for compositional analysis at each collection time. The RF ewes produced less milk than FF ewes (106 vs 137.4 g; P < .01) at 1100 on d 7, but yields of MB and SA ewes were similar. At 1700 on d 7, milk yield was only 15.9 g less (74.3 vs 90.2 g; P < .10) for RF than for FF ewes, but it was 26 g less (69.2 vs 95.2 g; P < .01) for MB than for SA ewes. On d 9, there was no significant difference in yields of RF and FF ewes; however, MB ewes continued to produce less milk than SA ewes (96.6 vs 125.4 g; P < .10). No significant interactions between feeding regimen and MB treatment were found for milk yield. These data provide evidence that MB treatment of ewes is effective in reducing milk production. Furthermore, even greater reduction can be achieved when MB is combined with RF.
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PMID:Reducing milk production in ewes at weaning using restricted feeding and methscopolamine bromide. 925 May 2

Neurons which release atrial natriuretic peptide (ANPergic neurons) have their cell bodies in the paraventricular nucleus and in a region extending rostrally and ventrally to the anteroventral third ventricular (AV3V) region with axons which project to the median eminence and neural lobe of the pituitary gland. These neurons act to inhibit water and salt intake by blocking the action of angiotensin II. They also act, after their release into hypophyseal portal vessels, to inhibit stress-induced ACTH release, to augment prolactin release, and to inhibit the release of LHRH and growth hormone-releasing hormone. Stimulation of neurons in the AV3V region causes natriuresis and an increase in circulating ANP, whereas lesions in the AV3V region and caudally in the median eminence or neural lobe decrease resting ANP release and the response to blood volume expansion. The ANP neurons play a crucial role in blood volume expansion-induced release of ANP and natriuresis since this response can be blocked by intraventricular (3V) injection of antisera directed against the peptide. Blood volume expansion activates baroreceptor input via the carotid, aortic and renal baroreceptors, which provides stimulation of noradrenergic neurons in the locus coeruleus and possibly also serotonergic neurons in the raphe nuclei. These project to the hypothalamus to activate cholinergic neurons which then stimulate the ANPergic neurons. The ANP neurons stimulate the oxytocinergic neurons in the paraventricular and supraoptic nuclei to release oxytocin from the neural lobe which circulates to the atria to stimulate the release of ANP. ANP causes a rapid reduction in effective circulating blood volume by releasing cyclic GMP which dilates peripheral vessels and also acts within the heart to slow its rate and atrial force of contraction. The released ANP circulates to the kidney where it acts through cyclic GMP to produce natriuresis and a return to normal blood volume.
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PMID:Neuroendocrine regulation of salt and water metabolism. 925 61

Neurons containing neural nitric oxide synthase (nNOS) are found in various locations in the hypothalamus and, in particular, in the paraventricular and supraoptic nuclei with axons which project to the median eminence and extend into the neural lobe where the highest concentrations of NOS are found in the rat. Furthermore, nNOS is also located in folliculostellate cells and LH gonadotropes in the anterior pituitary gland. To define the role of NO in the release of hypothalamic peptides and pituitary hormones, we injected an inhibitor of NOS, Ng-monomethyl-L-arginine (NMMA) or a releasor of NO, nitroprusside (NP) into the third ventricle (3V) of conscious castrate rats and determined the effect on the release of various pituitary hormones. In vitro, we incubated medial basal hypothalamic (MBH) fragments and studied inhibitors of NO synthase and also releasors of NO. The results indicate that NOergic neurons play an important role in stimulating the release of corticotrophin-releasing hormone (CRH), luteinizing hormone releasing-hormone (LHRH), prolactin-RH's, particularly oxytocin, growth hormone-RH (GHRH) and somatostatin, but not FSH-releasing factor from the hypothalamus. NO stimulates the release of LHRH, which induces sexual behavior, and causes release of LH from the pituitary gland. The intrahypothalamic pathway by which NO controls LHRH release is as follows: glutamergic neurons synapse with noradrenergic terminals in the MBH which release nonepinephrine (NE) that acts on alpha 1 receptors on the NOergic neuron to increase intracellular free Ca++ which combines with calmodulin to activate NOS. The NOS diffuses to the LHRH terminal and activates guanylate cyclase (GC), cyclooxygenase and lipoxygenase causing release of LHRH via release of cyclic GMP, PGE2 and leukotrienes, respectively. Alcohol and cytokines can block LHRH release by blocking the activation of cyclooxygenase and lipoxygenase without interfering with the activation of GC. GABA also blocks the response of the LHRH neurons to NO and recent experiments indicate that granulocyte macrophage colony-stimulating factor (GMCSF) blocks the response of the LHRH neuron to NP by activation of GABA neurons since the blockade can be reversed by the competitive inhibitor of GABAa receptors, bicuculine.
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PMID:The role of nitric oxide (NO) in control of hypothalamic-pituitary function. 939 93

Dysfunction of various hypothalamic systems may be the basis of a number of symptoms in Prader-Willi syndrome. The often abnormal position of the baby in the uterus at the onset of labour, the high percentage of infants with asphyxia and the high proportion of children born prematurely or post-maturely may all be related to abnormal fetal hypothalamic systems, as the fetal hypothalamus plays a crucial role in labour. Abnormal luteinizing hormone-releasing hormone neurones are thought to be responsible for the decreased levels of sex hormones, resulting in non-descended testes, undersized sex organs and insufficient growth during puberty. A lack of growth hormone-releasing hormone may also contribute to the short stature of patients with Prader-Willi syndrome. In addition, the aberrant control of body temperature and daytime hypersomnolence may result from hypothalamic disturbances. The number of oxytocin neurones--the putative satiety neurones--in the hypothalamic paraventricular nucleus is markedly decreased in Prader-Willi syndrome. This is presumed to be the basis of the insatiable hunger and obesity of patients with the syndrome.
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PMID:Prader-Willi syndrome and the hypothalamus. 940 39

The adipose tissue-derived hormone leptin regulates body weight homeostasis by decreasing food intake and increasing energy expenditure. The weight-reducing action of leptin is thought to be mediated primarily by signal transduction through the leptin receptor (LR) in the hypothalamus. We have used immunohistochemistry to localize LR-immunoreactive (LR-IR) cells in the rat brain using an antiserum against a portion of the intracellular domain of LR that is common to all LR isoforms. The antiserum recognized the short and long isoforms of LR in transfected hematopoietic BaF3 cells. To examine the chemical nature of target cells for leptin, direct double-labeling immunofluorescence histochemistry was applied. The results show extensive distribution of LR-like immunoreactivity (LR-LI) in the brain with positively stained cells present, e.g., in the choroid plexus, cerebral cortex, hippocampus, thalamus, and hypothalamus. In the hypothalamus, strongly LR-IR neurons were present in the supraoptic nucleus (SON) and paraventricular nucleus (PVN), periventricular nucleus, arcuate nucleus, and lateral hypothalamus. Weaker LR-IR neurons were also demonstrated in the lateral and medial preoptic nuclei, suprachiasmatic nucleus, ventromedial and dorsomedial nuclei, and tuberomammillary nucleus. Confocal laser scanning microscopy showed LR-LI in the periphery of individual cells. In magnocellular neurons of the SON and PVN, LR-LI was demonstrated in vasopressin- and oxytocin-containing neurons. In parvocellular neurons of the PVN, LR-LI was demonstrated in many corticotropin-releasing hormone-containing neurons. LR-IR neurons were mainly seen in the ventromedial aspect of the arcuate nucleus, where LR-LI co-localized with neuropeptide Y. In the ventrolateral part of the arcuate nucleus, LR-LI was present in many large adrenocorticotropic hormone-IR proopiomelanocortin-containing neurons and in a few galanin-, neurotensin-, and growth hormone-releasing hormone-containing neurons. In the dorsomedial arcuate nucleus, few tyrosine hydroxylase (dopamine)-containing neurons were seen to have LR-LI. Melanin-concentrating hormone-containing neurons in the lateral hypothalamus had LR-LI. Based on the immunohistochemical results, possible interactions of leptin with brain mechanisms are discussed.
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PMID:Leptin receptor immunoreactivity in chemically defined target neurons of the hypothalamus. 941 31

1. Studies of the regulation of neurosecretory cell gene expression suffer from the lack of suitable cell lines. Two approaches have been used to overcome this deficit: transfection of neuropeptide genes into heterologous cell lines and generation of transgenic animals. 2. Studies with heterologous cell lines have revealed the potential involvement of nuclear hormone receptors, POU proteins, and fos/jun/ATF family members in the regulation of the vasopressin and oxytocin genes. Although limited in their scope, these studies have contributed greatly to the dissection of basic properties of elements in the vasopressin and oxytocin gene promoters. 3. Transgenic mice, and more recently rats, have been used to elucidate genomic regions governing cell specificity and physiological regulation of neurosecretory gene expression. The genes encoding the neuropeptides vasopressin and oxytocin have been used in many transgenic studies, due to the well-defined expression patterns and physiology of the endogenous neuropeptides. Cell-specific and physiologically regulated expression of these transgenes has been achieved, demonstrating the action of putative repressor elements and regulation of the expression of one gene by sequences present in the other gene. 4. Appropriate expression and translation of transgenes have resulted in the production of several useful systems. Expression of oncogene sequences in gonadotropin-releasing hormone neurons has allowed the development of cell lines from the resulting tumors, overproduction of corticotropin-releasing factor has produced animal models of anxiety and obesity, and directed ectopic expression of growth hormone has generated a potentially useful rat model of dwarfism. These and other animal models of human disease will provide important avenues for the development of therapeutic strategies.
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PMID:Transgenic and transcriptional studies on neurosecretory cell gene expression. 953 88

Groups of 9 or 10 cows were assigned to one of three treatments 1) machine-milking three times daily, 2) machine-milking six times daily, and 3) suckling three times daily in addition to machine-milking three times daily. Treatments were conducted during the first 6 wk postpartum. During wk 5, digestibility of the diet was estimated by the indigestible neutral detergent fiber method. During wk 6, milk yield and dry matter intake (DMI) were recorded daily, and plasma concentrations of glucose, nonesterified fatty acids, urea, protein, growth hormone, insulin, insulin-like growth factor I, oxytocin, and prolactin were determined. Milk yields were 38.5, 46.8, and 52.7 kg/d, and DMI were 18.1, 21.2, and 17.2, for cows on treatments 1, 2, and 3, respectively. Plasma glucose concentrations decreased, and plasma nonesterified fatty acid concentrations increased, for cows on treatments 2 and 3 compared with cows on treatment 1. Digestibility of dry matter was 57.5, 60.5, and 60.6%; of organic matter was 62.6, 64.6, and 66.8%; and of crude protein was 59.3, 62.7, and 64.6% for cows on treatments 1, 2, and 3, respectively. Concentrations of all assayed hormones, except insulin, increased moderately for cows on treatment 2 compared with cows on treatment 1 and increased dramatically for cows on treatment 3. Insulin concentrations followed the opposite trend. The DMI were positively related to milk yields and negatively related to oxytocin concentrations. Digestibility was negatively related to plasma glucose concentrations in a nonlinear pattern. The possible involvement of hormones in improvement of digestibility is discussed.
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PMID:The effect of enhanced milk yield of dairy cows by frequent milking or suckling on intake and digestibility of the diet. 962 Dec 46


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