Showing papers on "Oxytocin published in 1987"
TL;DR: Results demonstrate that central OT may play an important role in stimulating maternal behaviour in the sheep and demonstrate that ewes spent significantly more time near a lamb in a cage following both 5- and 20-micrograms doses of OT.
Abstract: The maternal behaviour of 7 ovariectomized, oestrogen-treated ewes was recorded after intracerebroventricular (ICV) infusions of oxytocin (OT). At weekly intervals 10-min behaviour tests were given st
341 citations
TL;DR: Cryostat sections were cut through the hypothalamus of rats which had been given a 2% NaCl solution to drink for up to 12 days and resulted in a progressive increase of vasopressin, oxytocin and dynorphin mRNAs hybridized in the magnocellular neurones of the supraoptic and paraventricular nuclei.
Abstract: 1. Cryostat sections were cut through the hypothalamus of rats which had been given a 2% (w/v) NaCl solution to drink for up to 12 days. 2. In situ hybridization histochemistry was performed on these sections using synthetic oligonucleotide probes against part of the precursor sequence for vasopressin, oxytocin, dynorphin, enkephalin and corticotrophin-releasing factor (CRF). 3. Drinking 2% NaCl solution resulted in a progressive increase of vasopressin, oxytocin and dynorphin mRNAs hybridized in the magnocellular neurones of the supraoptic (s.o.) and paraventricular (p.v.) nuclei. No enkephalin mRNA was detected in the magnocellular areas of the control animals although small quantities of probe did hybridize after 12 days of salt loading and after the stress of I.P. hypertonic saline. 4. Ten-day-lactating female rats were also studied. They had a very marked increase in oxytocin mRNA with smaller increases of vasopressin and dynorphin mRNAs. No detectable enkephalin mRNA was hybridized in the magnocellular s.o. or p.v. nuclei and CRF mRNA was unchanged in both the s.o. nucleus and the p.v. nucleus.
331 citations
TL;DR: Using a monolayer primary culture of human placental cells, it is found that CRF stimulates secretion of peptides containing the ACTH sequence in the placenta in a dose-dependent manner, as it does in the pituitary.
Abstract: The hypothalamic-pituitary-adrenocortical axis is activated in pregnancy and parturition. Levels of immunoreactive corticotrophin releasing factor (irCRF), immunoreactive adrenocorticotropic hormone (irACTH) and cortisol concentrations in maternal plasma are elevated throughout gestation, increase further during labour and fall precipitously after parturition. The placenta contains biologically active CRF and ACTH and it has been suggested that the placenta produces these peptides during pregnancy. Here we show that irCRF is located in the cytotrophoblast cells of placenta collected at term. Using a monolayer primary culture of human placental cells we have found that CRF stimulates secretion of peptides containing the ACTH sequence in the placenta in a dose-dependent manner, as it does in the pituitary. This effect is reversed by a CRF antagonist and is mimicked by dibutyryl cyclic AMP and forskolin. Glucocorticoids, which suppress the secretion of pituitary ACTH, were found to have no influence on release of irACTH by the placenta. Oxytocin and prostaglandins stimulate irACTH and irCRF secretion from cultured placental cells and the irACTH-releasing activity of two prostaglandins is partially reversed by a CRF antagonist. Thus CRF may be involved in the paracrine regulation of placental irACTH secretion.
320 citations
TL;DR: It is concluded that in man AVP is secreted during sexual arousal, and there is, subsequently, a selective release of OT at the time of ejaculation.
Abstract: We measured plasma oxytocin (OT) and arginine vasopressin (AVP) concentrations in 13 normal men during sexual arousal and ejaculation. Mean plasma AVP increased from 1.4 ± 0.2 (±se) to 5.3 ± 1.7 pmol/L (P < 0.05) during arousal, but there was no significant change in OT. In contrast, at ejaculation mean plasma OT rose from a basal value of 1.4 ± 0.3 to 7.3 ± 0.6 pmol/L (P < 0.01) and then fell to basal concentrations in 30 min. AVP, however, had returned to basal levels at the time of ejaculation and remained stable thereafter. We conclude that in man AVP is secreted during sexual arousal, and there is, subsequently, a selective release of OT at the time of ejaculation.
298 citations
TL;DR: The effectiveness of oxytocin antagonist in suppressing the rapid onset of post-partum maternal behaviour supports the hypothesis that centrally released oxytocIn is involved in this process.
Abstract: Endogenous oxytocin released into the brain at parturition may stimulate the onset of maternal behaviour. In this study an attempt was made to block spontaneous maternal behaviour following natural delivery in Wistar rats by the injection of an antagonist of oxytocin into the cerebral ventricles. The analogue antagonist, d(CH2)5-8-ornithine-vasotocin, was administered by injection into a chronically implanted cannula in the right lateral ventricle at hourly intervals, beginning immediately after the expulsion of the first pup. The antagonist did not interfere with the normal progress of parturition or birth-related behaviours. After delivery of the last pup, mothers rested for 40 min in the test cage with the pups having been removed. Four pups and standard nesting material were then presented. Latency to pup carrying and duration of pup manipulation, nest building, and time spent on the nest with the pups, as well as duration of autogrooming and general activity were determined. Saline-injected controls started gathering the pups immediately and usually showed all elements of maternal behaviour within 10 min. Antagonist-treated mothers showed a marked delay in the onset of pup grouping and other maternal behaviours. At the end of 1 h, two out of six mothers had not yet picked up a single infant. Pups left overnight with their mothers were gathered into the nest and suckled, and no long-term effects of the antagonist were evident on retesting. The effectiveness of oxytocin antagonist in suppressing the rapid onset of post-partum maternal behaviour supports the hypothesis that centrally released oxytocin is involved in this process.(ABSTRACT TRUNCATED AT 250 WORDS)
261 citations
TL;DR: In the hypothalamus, no relationship can be established between the known effect of oxytocin on oxytoc inergic magnocellular neurons and detection of specific [3H]oxytocin-binding sites, and autoradiography apparently only reveals some of the Oxytocin receptors in the brain.
195 citations
TL;DR: Observations that the effects of CCK-8 on OXY release were attenuated by gastric vagotomy clearly demonstrate the existence of a sensitive neural link between the stomach and the neurohypophysis in the rat.
Abstract: Systemic administration of cholecystokinin octapeptide (CCK-8) prompts an abrupt increase in circulating levels of oxytocin (OXY) but not vasopressin (VP) in rats. The present study determined whether CCK-8 selectively stimulated OXY-secreting neurons in the hypothalamic supraoptic nucleus of pentobarbital-anesthetized male rats. Antidromically identified neurosecretory neurons were categorized into putative OXY- and VP-secreting cells on the basis of their firing patterns and response to peripheral baroreceptor activation. Of 36 OXY-secreting cells studied, 30 demonstrated a 50-200% increase in firing frequency within 2 min of administering CCK-8 by intravenous or intraperitoneal injection, whereas none of the eight VP-secreting neurons studied was activated. In related experiments, 4-10 ml of air were used to inflate an intragastric balloon in rats; 20 of 22 OXY-secreting neurons displayed an abrupt and readily reversible increase in firing frequency, whereas only 2 of 17 VP-secreting cells were activated. Gastric distension similarly elevated plasma OXY levels in unanesthetized rats with indwelling gastric cannulas. Together with previous findings that the effects of CCK-8 on OXY release were attenuated by gastric vagotomy, these observations clearly demonstrate the existence of a sensitive neural link between the stomach and the neurohypophysis in the rat.
190 citations
TL;DR: In the behavioral despair test in mice, oxytocin, i.p. injected 60 min before testing, significantly reduced the duration of immobility at doses of 0.250-1.0 mg/Kg; the effect being similar to that of imipramine.
187 citations
TL;DR: This hypothesis that this hypothalamic structure regulates gastric function through its peptidergic connections with medullary vagal structures is supported by the observations that injections of an oxytocin antagonist into the DMN produced a disinhibition of gastric motility and an increase in the motility evoked by subsequent PVN stimulation.
175 citations
TL;DR: The similarities and differences between vasopressin or oxytocin receptors in the brain and peripheral receptors for these peptides are focused on.
Abstract: Publisher Summary This chapter focuses on the similarities and differences between vasopressin or oxytocin receptors in the brain and peripheral receptors for these peptides. The chapter also discusses the transduction mechanisms activated by vasopressin and oxytocin receptors in the brain and peripheral nervous system. Vasopressin and oxytocin meet most of the criteria that are applied to assign a role as a neurotransmitter or a neuromodulator to a given compound. It is recognized that vasopressin and oxytocin are synthesized at multiple sites in the brain in neurons projecting to several areas. A calcium-dependent release of oxytocin and (or) vasopressin can be evoked by potassium or veratridine in various extrahypothalamic areas of the brain. No direct effect of vasopressin on the adenylate cyclase activity of nervous tissue can be demonstrated. Vasopressin stimulates inositol lipid breakdown in hippocampal slices and isolated sympathetic ganglia.
164 citations
TL;DR: The results of this preliminary study support the concept of an increased concentration of uterine oxytocin receptors being aetiologically important in uncomplicated premature labour and suggest that the present Oxytocin antagonist could be an interesting therapeutic alternative in the condition, primarily because of the marked selectivity of its effect.
TL;DR: The results confirm the previous observations showing that the PVN has a crucial role in the expression of yawning and penile erection induced by dopamino-mimetic drugs and oxytocin, and suggest that ACTH-derived peptides induce the above responses by a mechanism not involving PVN hypothalamic dopamine or Oxytocin.
TL;DR: It is concluded that intracerebrally projecting OT systems may be activated during coitus and may contribute to the mechanisms underlying postejaculatory refractoriness.
TL;DR: It is concluded that nonapeptide levels are altered across late pregnancy and early postpartum in some hypothalamic synthesis sites and in certain limbic and brainstem sites.
Abstract: This study examines immunoreactive levels of oxytocin (OT) and arginine-vasopressin (AVP) from acid extracts of the paraventricular nucleus (PVN), supraoptic nucleus (SON), anterior commissural nucleus (ACN) and the suprachiasmatic nucleus (SCN) as well as selected extrahypothalamic sites in pregnant or postpartum (PP) rats. Animals are sacrificed between 08.30 and 10.30 h 16 or 22 days after sperm is detected in their vaginal smears or on the morning after parturition. Peptide levels of pregnant or PP animals are compared to levels of ovariectomized (OVXed) rats sacrificed and assayed simultaneously. OT immunoreactive levels in the PVN and SON are significantly elevated in late pregnancy and PP. OT content of the ACN is elevated on day 16, but drops to control levels by day 22 of pregnancy and day 1 PP. Concomitant with the falling OT content in the ACN at the end of pregnancy, samples from the ventral septum have significantly increased OT content on day 1 PP. In extracts including the nucleus of the tractus solitarius (NTS) and dorsal motor nucleus of the vagus (dMX) OT is also elevated on the day after parturition. AVP levels peak on the day before parturition in all hypothalamic nuclei examined. These increases are significantly greater than in OVXed controls in the PVN and SON. AVP levels in the lateral habenula are elevated both on day 16 of pregnancy and on the first day PP. From these data we conclude that nonapeptide levels are altered across late pregnancy and early postpartum in some hypothalamic synthesis sites and in certain limbic and brainstem sites. We also postulate that OT is transported out of the ACN to extrahypothalamic sites around the time of parturition.
TL;DR: The following sequence of events is suggested to occur at oestrogen-induced luteolysis: induction of the oxytocin receptor; increased turnover of phosphoinositides; onset of episodic secretion of PGF-2 alpha; and functional lutesolysis.
Abstract: Administration of oestradiol-17 beta benzoate on Days 9 and 10 of the oestrous cycle resulted in episodic secretion of PGF-2 alpha (as indicated by elevated circulating concentrations of 13,14-dihydro-15-ketoprostaglandin F-2 alpha) and a decline in circulating progesterone. Release of PGF-2 alpha began 35 +/- 3 h after first injection of oestrogen and progesterone concentrations declined from 42 +/- 3 h. Secretion of oxytocin, which was first observed 26 +/- 3 h after oestrogen treatment, preceded secretion of PGF-2 alpha; 69% of pulses of oxytocin coincided with episodes of PGF-2 alpha secretion. Uterine oxytocin receptor concentrations were raised in ewes treated with oestrogen, increases occurring in caruncular endometrium and myometrium by 12 h after treatment and in intercaruncular endometrium by 24 h. Raised receptor concentrations were followed at 24 h by increases in the incorporation of [3H]inositol into phosphatidylinositol and in the hydrolysis of labelled tissue phosphoinositides in response to oxytocin in slices of caruncular endometrium incubated in vitro. The following sequence of events is therefore suggested to occur at oestrogen-induced luteolysis: induction of the oxytocin receptor; increased turnover of phosphoinositides; onset of episodic secretion of PGF-2 alpha; and functional luteolysis.
TL;DR: Results demonstrate that OT gene expression in the magnocellular neurons of the SON, PVN, and anterior commissural nucleus is sensitive to this osmotic stimulus, as is the VP gene of magno cellular neurons in the Son and PVN.
Abstract: The effect of prolonged osmotic stimulation on the oxytocin (OT) mRNA levels of OT-producing neurons was investigated in separate hypothalamic nuclei of the rat. After drinking 2% NaCl for 2 weeks, a 2-fold increase in the OT mRNA content was found by Northern blot analysis of microdissected supraoptic nucleus (SON) and paraventricular nucleus (PVN). The same samples showed a similar change in vasopressin (VP) mRNA levels. This treatment resulted in a 70% depletion of both OT and VP from the neurointermediate lobe of the pituitary gland and a marked increase in OT and VP plasma levels. Analysis of the OT mRNA concentration by quantitative in situ hybridization showed that the SON, PVN, and anterior commissural nucleus responded similarly, with a 1.5-fold increase in OT mRNA after 7 days of osmotic stimulation. These results demonstrate that OT gene expression in the magnocellular neurons of the SON, PVN, and anterior commissural nucleus is sensitive to this osmotic stimulus, as is the VP gene of magnocellular neurons in the SON and PVN. The responsiveness of OT-producing neurons may point to a role for OT in the regulation of water and electrolyte balance.
TL;DR: In this article, after 8 days of salt loading to stimulate the hypothalamo-neurohypophyseal system, NADPHd activity is markedly increased in the posterior pituitary gland but not in the hypothalamus of rats.
TL;DR: The data support the hypothesis that the control of sodium appetite is governed by inhibitory as well as excitatory central mechanisms and suggest that sodium appetite may be inhibited by activity in the supraoptic and/or paraventricular nuclei, the location of the neurons responsible for the synthesis of oxytocin, and can be stimulated only when activity in those neurons is reduced.
Abstract: In the present experiments we examined neurohypophyseal hormone secretion in various models of sodium appetite in rats. Basal plasma levels of oxytocin were found to be low in sodium-deficient adrenalectomized rats and in intact animals treated daily with desoxycorticosterone acetate, both of which groups drank large amounts of NaCl solution, whereas basal plasma levels of arginine vasopressin were neither stimulated nor suppressed. Conversely, sodium appetite consistently was inhibited by treatments that stimulated pituitary oxytocin secretion. However, sodium appetite was not inhibited by administration of exogenous oxytocin, nor was it stimulated by administration of an oxytocin receptor antagonist. These and other results suggest that sodium appetite may be inhibited by activity in the supraoptic and/or paraventricular nuclei, the location of the neurons responsible for the synthesis of oxytocin, and can be stimulated only when activity in those neurons is reduced. Whatever the final neural pathway, our data support the hypothesis that the control of sodium appetite is governed by inhibitory as well as excitatory central mechanisms.
TL;DR: The results suggest that OXT exerts predominantly excitatory effects in the SON and that putative OXT cells are more likely to be affected than putative vasopressin cells.
TL;DR: It is suggested that apomorphine, but not ACTH-(1-24), induce penile erection and yawning by releasing oxytocin in some brain area by being antagonized in a dose-dependent manner.
TL;DR: The LOBEX-lactating rat is not refractory to PRL-releasing stimuli other than suckling and its hypothalamic DA and serotonergic systems are functionally intact.
Abstract: The aim of this study was to determine the role of the posterior pituitary in the regulation of PRL release during suckling. Lactating rats were subjectd to posterior pituitary lobectomy (LOBEX) or sham surgery (SHAM) and separation from pups in the evening; experimental manipulations and blood collection were performed the next morning. In the first experiment rats were divided into three groups: SHAM, LOBEX, and LOBEX treated with a vasopressin analog, l-desamino-8-Darginine vasopressin and oxytocin. Plasma PRL levels in SHAM rats increased 20- to 25-fold upon introduction of pups and remained elevated for the duration of suckling. In contrast, basal plasma PRL levels in LOBEX rats were 3- to 4-fold higher than in SHAM but suckling failed to induce a further increase. Treatment of LOBEX rats with l-desamino-8-D-arginine vasopressin and oxytocin reduced water consumption and allowed for milk ejection and milk intake by the pups but did not restore the suckling-induced rise in PRL. The second experiment t...
TL;DR: The hypothesis that the facilitation of lordosis in ovariectomized rats by centrally-administered oxytocin is progesterone-dependent is supported.
TL;DR: The significant neurohypophysial hormone secretion in response to both nausea-producing agents and CCK suggests that AVP secretion in monkeys, similar to OT secretion in rats, might reflect activation of central pathways mediating nausea and/or inhibition of food intake, even when overt illness is not produced.
Abstract: Administration of lithium chloride and copper sulfate to adult monkeys caused marked elevations in plasma vasopressin (AVP) levels without significant increases in plasma oxytocin (OT) levels. Emesis was produced in five of the seven animals given these agents, in support of nausea as the main stimulus to AVP release. A similar pattern of AVP release without OT release was found after administration of cholecystokinin (CCK). Although most monkeys vomited in response to 10 micrograms/kg of CCK, a significant increase in plasma AVP levels also was produced with a dose of 1 microgram/kg, which did not produce emesis in any animal. These findings are in marked contrast with previous results in rats, which indicated that lithium chloride, copper sulfate, and CCK each stimulated OT rather than AVP release. Despite this interspecies difference, the significant neurohypophysial hormone secretion in response to both nausea-producing agents and CCK suggests that AVP secretion in monkeys, similar to OT secretion in rats, might reflect activation of central pathways mediating nausea and/or inhibition of food intake, even when overt illness is not produced.
TL;DR: The analgesic effect of intraventricular somatostatin-14, arginine vasopressin (AVP), and oxytocin (OT) were tested in one terminally ill cancer patient with a diffuse mesothelioma suffering intractable continuous and incapacitating thoracic pain.
Abstract: The analgesic effect of intraventricular somatostatin-14 (SOM-14), arginine vasopressin (AVP), and oxytocin (OT) were tested in one terminally ill cancer patient with a diffuse mesothelioma suffering
TL;DR: Results suggest that, following electrical stimulation, oxytocin and vasopressin are released locally within the magnocellular nuclei even when blocking action potentials.
Journal Article•
TL;DR: During oestrus the response to Oxytocin decreased dramatically in mares receiving oxytocin on alternate days, and the response also declined after Day 16 in the non-pregnant mares that had daily injections of oxytocIn even though plasma progesterone remained elevated.
Abstract: In Exp. 1, 4 mares were given oxytocin intravenously (10 i.u./500 kg body wt) daily between Days 9 and 14 (Day 0 = day of ovulation) when pregnant and on Days 9-14, 16, 18, 20 when non-pregnant (not inseminated). In the non-pregnant mares the increase in plasma PGFM response to oxytocin was greater at Day 13 (235 +/- 54 pg/ml) than at Day 11 (113 +/- 38 pg/ml; P less than 0.05) and was maximum at Day 16. However, these animals did not return to oestrus and plasma progesterone did not fall below 4 ng/ml. There was no significant increase in response to oxytocin between Days 9 and 14 in the pregnant animals. In Exp. 2, when these same mares were challenged with oxytocin on alternate day (Days 9, 11 and 13 for pregnant mares, Days 9, 11, 13, 15, 17 and 19 for non-pregnant mares) there was a significant difference in the response between non-pregnant and pregnant mares by Day 13 (383 +/- 19 pg/ml vs 88 +/- 9 pg/ml; P less than 0.005). Plasma progesterone concentrations declined normally and the mares returned to oestrus. During oestrus the response to oxytocin decreased dramatically in mares receiving oxytocin on alternate days, and no response was seen by Day 19. The response also declined after Day 16 in the non-pregnant mares that had daily injections of oxytocin even though plasma progesterone remained elevated. The decreased response coincided with the increase in plasma oestrogen concentrations, suggesting that oestrogens play a role in the control of the response.(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: It is reported here that relaxin has a dual effect on neurohypophysial hormone secretion, under basal conditions, and when the nerve endings were depolarized, vasopressin and oxytocin secretion was potentiated.
Abstract: The hormone relaxin (for review see refs 1 and 2) has recently been shown to inhibit not only uterine muscle contraction3, but also the release of oxytocin into the plasma. Intravenous injection of porcine relaxin in anaesthetized lactating rats inhibits milk ejection and injection of relaxin into the cerebral ventricles disturbs the pattern of the milk ejection reflex4. Recent experiments performed in vivo indicate that relaxin might act not only in the uterus, but also in the hypothalamus and possibly in the neurohypophysis5. We tested this hypothesis in vitro by studying the effect of relaxin on hormone release from isolated neural lobes of the pituitary and isolated neurosecretory nerve endings of the neurohypophysis from the rat. We report here that relaxin has a dual effect on neurohypophysial hormone secretion. Under basal conditions, vasopressin and oxytocin release was inhibited by relaxin but, when the nerve endings were depolarized, vasopressin and oxytocin secretion was potentiated. We also found that relaxin acts at a stage before the increase in cytoplasmic free Ca2+ that is necessary for inducing hormone release, possibly by gating the calcium channel.
TL;DR: Evidence is provided for a direct membrane effect of oxytocin on a defined population of neurons in the rat brain and in the guinea pig brainstem, where homologous nuclei in the brains of two closely related mammals differ markedly in the density of Oxytocinergic axons they contain.
Abstract: Intracellular recordings were obtained from vagal neurons and their response to oxytocin was investigated in slices from the rat and the guinea pig brainstem. After recording, Lucifer yellow was injected into the cells to verify their localization within the dorsal motor nucleus of the vagus nerve (dmnX). In the rat, virtually all neurons throughout the rostrocaudal extent of the dmnX increased their rate of firing in the presence of 10-1000 nM oxytocin and their membrane depolarized in a reversible concentration-dependent manner. This excitation was probably exerted directly on the impaled cells rather than being synaptically mediated, since it persisted in a low calcium/high magnesium medium or in the presence of tetrodotoxin. These data provide evidence for a direct membrane effect of oxytocin on a defined population of neurons in the rat brain. In the guinea pig, vagal neurons were fired by glutamate but were not excited by oxytocin, even though we detected many more oxytocin-immunoreactive structures in the guinea pig dmnX than in the rat dmnX. Therefore, homologous nuclei in the brains of two closely related mammals differ markedly in the density of oxytocinergic axons they contain. Unexpectedly, the magnitude of the electrophysiological effects of oxytocin on vagal neurons appeared inversely related to the amount of oxytocin-like immunoreactivity present in dmnX.
Journal Article•
TL;DR: In this paper, a series of 1776 patients allowed to labor after a previous cesarean section, of whom 485 (27%) were treated with oxytocin were compared with those who did not, no significant differences were found with respect to uterine rupture, maternal morbidity, fetal morbidity or fetal mortality.