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

Measurements were made of the effects of intracerebroventricular treatment with beta-endorphin (BE; 100 ng) on the arginine-8-vasopressin (AVP) and oxytocin contents of rat hypothalamic and limbic brain areas (hippocampus, amygdala and septum). The hormone concentrations were determined by radioimmunoassay. The administration of BE resulted in a significant reduction of the AVP level in the amygdala in a naloxone-reversible manner. Naloxone (Nal) administered subcutaneously significantly increased the AVP content in the septum. The results revealed that BE and Nal had regionally specific effects on the activity of the vasopressinergic system but not on that of the oxytocinergic system in the brain.
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PMID:The effects of beta-endorphin on arginine-8-vasopressin and oxytocin levels in rat brain areas. 252 2

Neurophysins have been considered to be physiologically inert carrier proteins for the neurohypophysial hormones, oxytocin and vasopressin. We have observed that bovine neurophysin-II indirectly stimulates prolactin release in estradiol-primed male rats. The release of prolactin is regulated by a dual hypothalamic control system, the prolactin-release-inhibiting factor and the prolactin-releasing factor. We have tried to clarify whether neurophysin-II is acting through stimulation of prolactin-releasing factor by eliminating the possibility of dopaminergic prolactin release-inhibiting factor release. Male rats were primed with estradiol and functional dopaminergic prolactin release-inhibiting factor receptors were completely blocked by pretreatment with a large dose of pimozide (3 mg/kg), a dopaminergic receptor blocking agent. The neurophysin-II stimulated prolactin release in the rats which did not have any functional dopaminergic prolactin release-inhibiting factor receptors suggesting that neurophysin-II likely initiates a chain of events which eventually stimulates prolactin-releasing factor release since the possibility of involvement of the dopaminergic prolactin release-inhibiting factor system is eliminated. Opioids are known to be one of a chain of events which transmit external stress into a stimulation of prolactin release. Naloxone, a mu-receptor antagonist, was injected 20 min before neurophysin-II administration into rats which were primed with estradiol and pretreated with pimozide (3 mg/kg), but the naloxone administration did not block the prolactin release stimulated by neurophysin-II injection. This result indicates that opioids are not one of the chain of events between initiation of stimulation by neurophysin-II and prolactin release.
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PMID:Bovine neurophysin-II stimulates prolactin release without involvement of dopaminergic prolactin-release inhibiting factor receptor in the estradiol-primed male rat. 257 26

1. Coexisting with oxytocin or vasopressin in the cell bodies and nerve terminals of the hypothalamic-neurohypophysial system are smaller amounts of other peptides. For a number of these "copeptides" there is strong evidence of corelease with the major magnocellular hormones. Guided by the location of their specific receptors we have studied the effects of three copeptides, dynorphin, cholecystokinin (CCK), and corticotropin releasing hormone (CRH), on the secretion of oxytocin and vasopressin from isolated rat neural lobe or neurointermediate lobe preparations in vitro. 2. Dynorphin is coreleased with vasopressin from neural lobe nerve terminals and acts on neural lobe kappa-opiate receptors to inhibit the electrically stimulated secretion of oxytocin. Naloxone augments oxytocin release from the neural lobe in a manner directly proportional to the amount of vasopressin (and presumably dynorphin) released. 3. Cholecystokinin, coreleased with oxytocin by neural lobe terminals, has been shown to have high-affinity receptors located in the NL and to stimulate secretion of both oxytocin and vasopressin. CCK's secretagogue effect was independent of electrical stimulation and extracellular Ca2+ and was blocked by an inhibitor of protein kinase C. 4. CRH, coreleased with OT from the neural lobe, has receptors in the intermediate lobe of the pituitary, but not in the neural lobe itself. CRH stimulates the secretion of oxytocin and vasopressin from combined neurointermediate lobes but not from isolated neural lobes. Intermediate lobe peptides, alpha and gamma melanocyte stimulating hormone, induced secretion of oxytocin and vasopressin from isolated neural lobes. Their effect was, like that of CCK, independent of electrical stimulation and extracellular Ca2+ and blocked by an inhibitor of protein kinase C. 5. Among the CRH-producing parvocellular neurons of the paraventricular nucleus, in the normal rat, approximately half also produce and store vasopressin. After removal of glucocorticoid influence by adrenalectomy, virtually all of the CRH neurons contain vasopressin. 6. The two subtypes of CRH neurosecretory cells found in the normal rat possess different topographical distributions in the paraventricular nucleus, suggesting the possibility of differential innervation. Stress selectively activates the vasopressin containing subpopulation of CRH neurons, indicating that there are separate channels of regulatory input controlling the two components of the parvocellular CRH neurosecretory system.
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PMID:Coexisting peptides in hypothalamic neuroendocrine systems: some functional implications. 257 30

The effect of two doses of oxytocin (2 or 4 UI/kg i.p.) has been studied in the male Wistar rats, either preceded or not by a naloxone administration (10 mg/kg i.p.), on the response of the hypothalamus-pituitary-adrenal system, the latter being valued by changes produced in the plasmatic corticosterone levels. Oxytocin produced significant increases of the plasmatic corticosterone levels, this effect being stronger and longer lasting after the superior dose. Naloxone alone produced the same effect, but not as intense and stable as that of oxytocin. Pretreatment with naloxone modified the response of the hypothalamus-pituitary-adrenal system to oxytocin, producing partial blockade. The results suggest that the oxytocin action on the hypothalamus-pituitary-adrenal axis might be mediated by the endogenous opiates.
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PMID:[Effect of oxytocin and naloxone on the plasma levels of corticosterone in the rat]. 263 Nov 54

The identity of the subtype of opioid receptor mediating morphine dependence in relation to oxytocin neurones was investigated. Virgin female rats were implanted with a subcutaneous osmotic minipump to infuse morphine continuously (up to 50 micrograms/h) into a lateral cerebral ventricle. After 5 days of morphine infusion, rats were anesthetized with urethane, and the electrical activity of electrophysiologically identified supraoptic neurones was recorded extracellularly while opioid antagonists were injected i.v. Putative oxytocin cells were excited following low doses of naloxone HCl: 4/7 cells were excited by 1 microgram/kg, 6/7 cells by 2.5 micrograms/kg, and 11/13 cells by doses of 5-50 micrograms/kg. MR2266 ((-)-5,9 alpha-diethyl-2-(3-furylmethyl)-2'-hydroxy-6,7-benzomorphan: an antagonist with much greater affinity for kappa-subtype opioid receptors than naloxone) excited oxytocin cells less potently: none of 9 cells was excited by 10 micrograms/kg MR2266, 2/4 cells were by 25-50 micrograms/kg, 3/9 cells by 100 micrograms/kg and only 4/8 by 200-500 micrograms/kg. At low concentrations naloxone is selective for mu-subtype opioid receptors, hence the morphine dependence of oxytocin neurones is probably via mu-receptors. Naloxone methylbromide (MRZ), a quaternary ammonium derivative of naloxone, excited oxytocin cells in morphine-treated rats, but was at least 10 times less potent than naloxone. Thus part of the morphine-withdrawal excitation of oxytocin neurones may be mediated by mu-receptors outside the blood-brain barrier.
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PMID:Sensitivity of magnocellular oxytocin neurones to opioid antagonists in rats treated chronically with intracerebroventricular (i.c.v.) morphine. 271 89

We investigated whether a sustained increase in oxytocin secretion, with or without enhanced electrical activity of the cell-bodies of oxytocin neurones, leads to a rapid increase in oxytocin mRNA content in these neurones. To stimulate oxytocin release, naloxone (2.5 mg/kg i.v. twice, 30 min apart) was given to urethane-anaesthetized female rats after intracerebroventricular (i.c.v.) morphine or vehicle infusion for 5 days; in the latter, naloxone acts on the neurohypophysis to increase oxytocin release without affecting the electrical activity of oxytocin neurone cell-bodies, but in the former, naloxone acts both on the neucohypophysis and on the cell-bodies to excite them electrically. Oxytocin content in peripheral plasma was measured intermittently by radioimmunoassay for 4 h after i.v. naloxone or vehicle, then the brain was removed and cryostat sections were cut through the supraoptic nucleus (SON). Oxytocin mRNA content in individual neurones (25-50 per rat) was measured semiquantitatively by in situ hybridisation histochemistry, using a tritiated synthetic cDNA 25-mer oligonucleotide probe, autoradiographical visualisation, and computer-assisted image-analysis to measure silver grain density. Nalaxone increased oxytocin content in plasma 7-fold for at least 40 min in i.c.v. vehicle-infused rats, and 40-fold for at least 40 min in i.c.v. morphine-infused rats. Naloxone had no significant effect on the oxytocin mRNA content in labelled cells in the SON, and no effect on the proportion of labelled cells, in either the i.c.v. morphine- or i.c.v. vehicle-infused rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Does acute, intense stimulation of oxytocin neurones in the supraoptic nucleus increase their content of oxytocin mRNA? 274 58

Oxytocin secretion is inhibited by opioids, and oxytocin is important in parturition. The effects on parturition of morphine, a relatively selective mu-opioid receptor agonist, were studied in the rat. Morphine or vehicle with or without the opiate antagonist naloxone were administered immediately after the birth of the second pup and the subsequent course of parturition was recorded in a total of 80 rats. Both s.c. morphine (10 mg/kg) and intracerebroventricular (i.c.v.) morphine (18 micrograms through a previously implanted cannula) interrupted parturition, delaying the birth of the sixth pup after treatment to 187.3 +/- 35.9 (S.E.M.) min and 195.4 +/- 19.5 min respectively, compared with 46.4 +/- 3.7 and 66.1 +/- 17.5 min after vehicle alone. The dose of morphine given i.c.v. had no effect when given s.c. Naloxone given concurrently prevented the effects of morphine. Eventually the rate of parturition in the morphine-treated groups recovered. Perinatal pup mortality rate was not increased when morphine was given to the mothers, but it did inhibit the expression of normal intrapartum maternal behaviour. Pup mortality was increased 48 h post partum by morphine given during parturition, and it reduced the proportion of rats with normal maternal behaviour 24 h post partum. Morphine did not affect spontaneous or oxytocin-stimulated contractile activity of the parturient uterus in vitro. The concentration of oxytocin in trunk blood plasma was decreased 40 min after i.c.v. morphine (24.3 +/- 3.9 vs 39.3 +/- 6.5 pmol/l in controls), as was vasopressin (7.2 +/- 1.5 vs 19.7 +/- 4.5 pmol/l in controls). Intravenous infusion of oxytocin (2-5 mU/min for 144.3 +/- 8.2 min; total infused 448.5 +/- 61.9 mU) after i.c.v. morphine re-started parturition; all pups were born to these rats (mean time to pup 6, 110.3 +/- 12.7 min) before the i.v. vehicle-infused rats given i.c.v. morphine re-started (mean time to pup 6, 406.3 +/- 125.2 min). It is concluded that morphine given during parturition acts centrally through opioid receptors to inhibit oxytocin secretion, and impairs the expression of maternal behaviour. Reversal of the effects of morphine on parturition by i.v. oxytocin demonstrates the important role of oxytocin in fetus ejection and expulsion.
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PMID:Interruption of parturition in rats by morphine: a result of inhibition of oxytocin secretion. 275 76

Naloxone increased the electrically (15 Hz, 1 min) evoked release of oxytocin from isolated neural lobes of rats 3-4-fold. In the presence of 4-aminopyridine or tetraethylammonium ions the evoked release of oxytocin was increased 8-9-fold and remained unaffected by naloxone. Increasing the calcium concentration in the medium from 1.2 to 3 mM caused only a marginal increase of the evoked oxytocin release. In conclusion, blockade of potassium channels and/or the resulting prolongation of the action potential can surmount the opioid inhibition of oxytocin release.
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PMID:Tetraethylammonium ions and 4-aminopyridine prevent opioid inhibition of neurohypophysial oxytocin release. 282 94

We have investigated the importance of endogenous opioids in the differential control of neurohypophysial peptide secretion. The effect of the opioid antagonist naloxone on the vasopressin and oxytocin responses to insulin-induced hypoglycemia was studied in 14 male subjects. Either saline (N = 8) or naloxone (4 mg bolus + 6 mg/h, N = 6) was infused iv during the study. After 60 min infusion soluble insulin 0.15 U/kg was injected. Naloxone infusion for 60 min did not alter basal plasma AVP or OT levels. Insulin-induced hypoglycemia led to a significant rise in plasma AVP in both saline and naloxone-infused subjects (P less than 0.05), which was maximal 45 min after insulin. There was no significant difference in the plasma AVP response to hypoglycemia between the 2 groups. Saline-infused subjects did not show any change in plasma OT in response to hypoglycemia whilst during concurrent naloxone infusion there was a significant rise in OT from 1.9 +/- 0.4 pmol/l before insulin to 3.2 +/- 1.3 pmol/l at 45 min (P less than 0.05). We conclude that there is opioid-mediated inhibition of OT which prevents its release when AVP is secreted in response to insulin-induced hypoglycemia.
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PMID:Opioid-mediated inhibition of oxytocin during insulin-induced hypoglycemic stimulation of vasopressin in man. 283 96

The influences of opioids on oxytocin secretion and parturition were investigated in the rat. Morphine, administered centrally or peripherally, severely delays the course of established parturition. This delay is accompanied by reduced plasma oxytocin levels and is overcome by treatment either with the opioid antagonist naloxone, or by infusion of oxytocin. An endogenous opioid regulatory mechanism inhibiting oxytocin secretion becomes activated immediately prior to and during parturition. This mechanism does not operate earlier in pregnancy or during normal lactation and is not seen in nonpregnant animals. Naloxone acutely speeds up the course of established parturition, an effect accompanied by greatly elevated plasma oxytocin levels. The mechanisms underlying opioid regulation of oxytocin neurones were investigated at two sites. Precipitated withdrawal from chronic morphine treatment causes hypersecretion of oxytocin. This response is mediated by greatly enhanced electrical activity in the perikarya of oxytocin neurones indicating the presence of opioid receptors on oxytocin neurones and/or on their afferent input. Opioid receptors are also present in the neurohypophysis where they exert direct and noradrenaline mediated effects on secretion from oxytocin terminals in vitro.
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PMID:Hypothalamic opioid mechanisms controlling oxytocin neurones during parturition. 284 5


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