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)

Neonatal treatment with monosodium glutamate (MSG) induces severe neuronal damage in selected brain areas, which in turn results in a number of neuroendocrine abnormalities during adult life. The present study was designed to determine what effects this partial and selective denervation of the hypothalamic-pituitary axis may have on the sensitivity of two key components of that axis, the median eminence (ME) and the anterior pituitary (AP). In order to test any changes in response that may occur after MSG treatment, the release of several peptide hormones from either the ME or the AP was evaluated in vitro, employing specific or general secretagogues. Male newborn pups of the Holtzman strain were injected with MSG every other day for 5 days, starting on day 2 of life; littermate controls received an injection of 10% NaCl. All animals were used when adult, at about 5-7 months of age. After decapitation, ME and AP tissues from control and MSG-treated rats were dissected out and incubated in vitro. Release of LHRH, SRIF, arginine vasopressin, and oxytocin from the ME was measured by direct RIA, under basal conditions and after stimulation with high K+ medium (28 mM). The results clearly indicate a marked hyperresponse of the release of each of the four neuropeptides by ME fragments from MSG-lesioned animals. The altered release was not attributable to changes in ME peptide content. In the case of the AP, the release of ACTH, LH, PRL, and GH in response to high K+ or, in some cases, to specific releasing factors, was evaluated in a dispersed cell preparation. The release of all four protein hormones was increased by high K+, and again the MSG-lesioned rats showed a pronounced hyperresponse. Corticotropin-releasing factor, at concentrations of 10(-9) and 10(-8) M enhanced ACTH release from control and MSG-lesioned rats, but the latter presented a marked hyperresponse. A similar observation on LH release was seen after stimulation with LHRH (10(-9) M). The results indicate that the neuronal damage induced by neonatal MSG treatment results in a generalized hyperresponsiveness in vitro to either specific or general secretagogues by ME or AP tissues, which may suggest the development of a denervation-type supersensitivity in the hypothalamic-pituitary axis. Since the release of these peptide hormones is sluggish in MSG-lesioned rats under in vivo conditions, it seems plausible to conclude that the major defect after the neurotoxin damage may reside in the loss of neurotransmitter systems normally innervating and regulating the activity of the peptidergic neurons.
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PMID:Increased responsiveness of the hypothalamic-pituitary axis after neurotoxin-induced hypothalamic denervation. 614 82

To determine whether oxytocin (OT) could alter the release of PRL and other hormones from the anterior pituitary gland, the effects of OT were examined in two in vitro and two in vivo test systems. Cells dispersed from anterior pituitary glands of intact adult male rats were incubated in medium containing OT at doses of 10(-8), 10(-7), 10(-6), and 10(-5) M in two trials. OT stimulated PRL release 1.5-fold (P less than 0.01) and 2- to 3-fold (P less than 0.001) above control levels at 10(-8) and 10(-7) M doses, respectively, thus indicating a dose-dependent relationship. Higher doses did not produce a further elevation above that obtained with 10(-7) M OT. Arginine vasopressin (AVP) caused a slight decrease in PRL release from dispersed cells while TRH produced a small (25%), significant, but nondose-related increase in PRL release. Hemipituitary glands from adult male rats, incubated with 10(-6) and 10(-5) M OT, released twice as much PRL (P less than 0.01) into the medium as paired controls, but 10(-7) M OT was ineffective. The iv injection of 1 or 10 micrograms OT into conscious male rats elevated plasma PRL by 50% (P less than 0.05) or 500% (P less than 0.001), respectively, above basal values at 5 min only. Vehicle or 0.1 microgram OT were without effect. When 0.1 microgram OT was microinjected into the third ventricle (3V) of conscious male rats, it paradoxically reduced plasma PRL by 40% at 30 min (P less than 0.05), whereas 1 microgram OT significantly lowered PRL at 5-60 min, with the maximum suppression (60%, P less than 0.001) occurring at 30 min. These latter findings may indicate that an ultrashort loop feedback mechanism exists whereby exogenous OT decreases hypothalamic OT secretion, thereby reducing the OT stimulus for PRL release. The specificity of the OT effect on PRL was attested to by the failure of OT to alter significantly FSH, LH, and TSH in each system. GH was unchanged except that 3V-injected OT (1 microgram only) elevated (P less than 0.001) plasma GH at 15-30 min. These results support the view that OT acts directly on the cells of the anterior pituitary gland at low to high doses to release PRL specifically and in a dose-related fashion. In contrast, 3V injection of OT reduces PRL secretion, thereby suggesting that OT may decrease its own neurosecretion by ultrashort loop feedback and thus reduce an OT stimulus for PRL release.
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PMID:Hypothalamic and pituitary sites of action of oxytocin to alter prolactin secretion in the rat. 640 33

Plasma oxytocin and PRL were measured in serial samples of blood collected from lactating rabbits nursing five to seven (mean, six) young on a once-daily suckling regimen. Each suckling episode lasted 4.0 +/- 1.1 (+/- SD) min on the average. Samples were obtained by means of an indwelling cardiac catheter before and 1, 3, 5, 10, 20, 30, and 60 min after suckling began. Measurements were performed at several stages of early, mid-, and late lactation. Oxytocin levels rose to peak values during suckling and declined rapidly after suckling stopped. PRL levels, on the other hand, did not reach peak values until 1-5 min after suckling had stopped, at which time plasma PRL concentrations plateaued and, in early and midlactation, were sustained at peak levels for 2-3 h; in late lactation, PRL secretion was not sustained after suckling had ceased. Peak PRL levels were relatively constant throughout most of lactation, with no significant differences between groups until late in lactation, when peak levels fell rather abruptly from a mean of 74 +/- 33.5 to 10.5 +/- 13.3 (+/- SD) ng/ml around day 25 in spite of a constant number of young and constant suckling frequency. Suckling failed to elicit any PRL release on day 30, but the administration of fluphenazine, a dopamine antagonist, did cause a rise in plasma PRL. Oxytocin release increased with advancing lactation, rising, on the average, 40 pg/ml on day 2 and to 250 and 490 pg/ml in mid- and late lactation, respectively. Dopaminergic agonist and antagonist drugs given to the doe before the nursing episode did not influence oxytocin release in response to suckling. Without a rise in plasma oxytocin, the young obtained no milk, but above a threshold level, there was no significant correlation between peak oxytocin levels and milk yield. When suckling failed to induce PRL secretion, milk secretion ceased rapidly in spite of copious oxytocin secretion. The failure of suckling to induce PRL release in late lactation, therefore, appears to be an important factor in the cessation of lactation.
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PMID:Release of oxytocin and prolactin by suckling in rabbits throughout lactation. 669 Feb 86

PRL release, milk ejection, and electroencephalographic states of sleep were monitored in conscious, lactating Holtzman rats. Plasma PRL levels were low in rats separated from their litters, but they increased when pups were returned to the cage, attached to the nipples of the mother, and suckled. The pups emitted ultrasonic vocalizations upon their return to the cage and before their attachment to the nipples. Exposure of mothers to the vocalizations of pups, whereas nipple attachment was prevented, failed to increase PRL release. In confirmation of previous work, milk ejection did not occur until the suckled mother exhibited electroencephalographic signs of sleep, and milk ejection could be inhibited if sleep was prevented. In contrast, sleep was not a prerequisite for PRL release and sleep deprivation of suckled mothers could not inhibit release of PRL. In summary, suckling-induced release of PRL was followed by an increased incidence of sleep and then by milk ejection. It is hypothesized that the rise in plasma PRL induces the sleep necessary for the reflex release of oxytocin required for milk ejection.
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PMID:Relationship of prolactin release in lactating rats to milk ejection, sleep state, and ultrasonic vocalization by the pups. 669 Feb 94

We have compared the effectiveness of TRH and a rat hypothalamic PRL-releasing factor (PRF; previously incubated with rat serum to destroy TRH) in stimulating the release of PRL into the plasma of conscious lactating rats when injected before and after pituitary PRL had been depleted and transformed into releasable PRL by 10 min of suckling. TRH (1.25 microgramsss) and PRF [equivalent to 2.5 stalk median eminence (SME) fragments] each caused a small increase (38 and 30 ng, respectively) in the plasma PRL concentration within 10 min when injected into nondepleted mothers. The levels then fell quickly. Suckling, by comparison, caused a sustained 175 ng/ml increase above basal levels. Though PRL depletion occurred, as expected, as a result of suckling, there was no measurable depletion within the pituitaries of TRH- or PRF-injected rats. By contrast, the iv administration of TRH (doses ranging from 2-250 ng) and hypothalamic PRF (doses ranging from 0.2-1.0 SME equivalent) after depletion-transformation had been effected by 10 min of suckling resulted in a rapid and, in most instances, a sustained elevation in the plasma PRL concentration comparable to that seen after suckling. Dose-response relationships, though, were not clearly evident with either PRF or TRH. Neither saline, 1.25 microgram TRH previously incubated in serum, 50 mU oxytocin, 1 microgram dopamine, 25 microgram LHRH, nor an extract of cerebral cortex prepared in the same manner as hypothalamic TRH caused plasma PRL to rise after PRL depletion. We conclude that TRH and possibly a separate hypothalamic PRF have a stimulatory action upon the releasable, but not upon the depletion-transformation, phase of PRL secretion in the lactating rat.
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PMID:Evidence that thyrotropin-releasing hormone and a hypothalamic prolactin-releasing factor may function in the release of prolactin in the lactating rat. 677 47

Serial plasma oxytocin (OT), PRL, TSH, FSH, LH, estrone, estradiol, and progesterone were measured by RIA in 12 women before and during a 30-min breast-feeding period on the third or fifth postpartum day. Plasma OT increased significantly from 10.8 +/- 3.4 to 22.4 +/- 3.5 pg/ml (mean +/- SE) within 2 min of suckling (P = less than 0.05) to reach the mean peak level of 53.2 pg/ml at 10 min. The increase in plasma OT was bimodal. Plasma PRL and TSH also increased significantly from baseline levels of 192 +/- 39 ng/ml and 16.9 +/- 5.6 microU/ml, respectively, to reach maximum levels of 427 +/- 91 ng PRL/ml at 10 min (P = less than 0.025) and 281.5 +/- 56.6 microU TSH/ml at 25 min (P = less than 0.005). Plasma FSH-beta (range of means, 3.5-4.6 ng/ml), LH (range of means, 1.7-2.6 mIU/ml), and estradiol (range of means, 29.8-38.2 pg/ml) were low and remained unchanged throughout breast feeding. Plasma progesterone was 6.0 +/- 0.4 ng/ml before breast feeding and did not alter significantly during breast feeding. The significance of these findings is discussed in relation to the milk let-down reflex and the relationship of TSH to PRL.
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PMID:Oxytocin release and plasma anterior pituitary and gonadal hormones in women during lactation. 678 15

Histamine administered intraperitoneally increased, in a dose-dependent manner, AVP, OXT and PRL levels in plasma of rats, whereas alpha-MSH levels were not affected. Levels of AVP in plasma after histamine 20.0 mg/kg treatment were approximately 100-fold higher than those of controls, while OXT and PRL levels were approximately 7-fold higher after this treatment. CSF content of AVP, OXT, PRL and alpha-MSH was not influenced by histamine, indicating that a stimulated release of hormones from the pituitary into the blood is not accompanied by a concomitant increase of secretion of these hormones into the CSF. Convulsions induced by pentylenetetrazol were accompanied by a temporary increase in AVP levels and by strongly and consistently elevated OXT levels in plasma. PRL and alpha-MSH plasma levels were affected in a biphasic manner. A convulsion type 1 induced elevated PRL levels and diminished alpha-MSH levels, while a convulsion type 2 had no effect on plasma PRL concentration, but increased the concentration of alpha-MSH. Only the level of OXT in CSF was increased after a pentylenetetrazol-induced convulsion type 1. The present data suggest that histamine affects the release of AVP, while pentylenetetrazol might act more specifically on the OXT-releasing system. Furthermore, a possible relationship between the pentylenetetrazol-induced increase of OXT levels in the CSF and amnesia is suggested.
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PMID:Hypophyseal hormone levels in blood and cerebrospinal fluid in response to histamine and pentylenetetrazol. 715 99

The effect of nursing on plasma levels of oxytocin (OT), arginine vasopressin (AVP), and PRL was studied in six normal women 2-3 days post partum. Maternal blood samples were obtained for measurement of OT, AVP, PRL, sodium, and osmolality 3 and 0 min before suckling, at 3-min intervals for 15 min during suckling, and 5 min after completion of suckling. Plasma OT rose during suckling from a mean (+/- SEM) baseline value of 1.1 +/- 0.2 to 3.6 +/- 0.6 microU/ml by 3 min (P < 0.001), reached a peak level of 6.4 +/- 1.5 microU/ml by 6 min (P < 0.005), and remained elevated for the entire 15-min period of suckling. Serial measurements of plasma OT during suckling failed to show a pattern consistent with episodic secretion. The baseline plasma AVP concentration was 0.4 +/- 0.1 microU/ml and was not significantly altered by suckling. Plasma sodium and osmolality remained unchanged during the suckling period. The baseline serum PRL level was 268 +/- 24 ng/ml and rose to 362 +/- 31 ng/ml after 15 min of suckling (P < 0.05). The data suggest that suckling is a specific stimulus for OT and PRL secretion but has no effect on AVP release.
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PMID:The effect of nursing on neurohypophyseal hormone and prolactin secretion in human subjects. 741 69

The hypothalamic neuropeptide oxytocin (OT) stimulates the release of several pituitary hormones, including ACTH, LH, and PRL. Although specific OT receptors have been identified in anterior pituitary membranes, the structure and cellular localization of these binding sites have not been elucidated. We previously cloned a rat OT receptor (OTR) gene and showed that its expression in rat uterus results in several transcripts ranging in size from 2.9-6.7 kilobases. In this study we show, by using Northern blot analysis, reverse transcriptase-polymerase chain reaction, and ultrastructural in situ hybridization that the same OTR gene is also expressed in the pituitary, where it gives rise to a 6.7- and a 4.8-kilobase messenger RNA. Ultrastructural in situ hybridization combined with immunogold labeling indicated that pituitary OTR gene expression is highly cell-specific and restricted to lactotrophs. In accordance with this finding, only the lactotroph-derived cell line MMQ expressed the OTR gene among several pituitary cell lines tested. Northern blot analysis, reverse transcriptase-polymerase chain reaction, and in situ hybridization analysis indicated a dramatic increase in pituitary OTR gene expression at the end of gestation and after estrogen treatment. Our results suggest that the OT effect on lactotrophs is direct, whereas OT actions on gonadotrophs and corticotrophs are either indirect or mediated via different receptors. Moreover, our findings imply that OT exerts its full potential as a physiological PRL-releasing factor only towards the end of gestation, and that therefore the role of OT as a hypothalamic PRL-releasing factor may so far have been underestimated.
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PMID:Oxytocin receptor messenger ribonucleic acid: characterization, regulation, and cellular localization in the rat pituitary gland. 754 May 44

To examine whether an excitatory amino acid (EAA) neurotransmitter may influence the secretion of oxytocin (OT), agonists and antagonists selective for three major groups of EAA receptors were microinjected into the area of right supraoptic nucleus (SON) of conscious unrestrained lactating rats. An increase in plasma OT concentration was induced by the EAA receptor agonist R,S-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and kainic acid, but not by agonists at other EAA receptors, such as N-methyl-D-aspartic acid (NMDA) or the metabotropic agonist (1S,3R)-1-amino-cyclopentane-1,3-dicarboxylic acid. Increasing AMPA doses between 0.1-0.8 nmol/SON progressively increased the percentage of animals showing OT discharges to 100% at the highest dose, whereas the responding animals showed similar elevations of plasma OT regardless of dose. OT release induced by intra-SON AMPA was prevented by treatment with the selective non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione, but not by antagonists of the NMDA receptor. Administration of this antagonist in the third ventricle blocked the release of OT and PRL induced by suckling. The L-type Ca2+ channel antagonist nimodipine and the Na+ channel inhibitor 3-amino-N-(aminoiminomethyl)5-(N-ethyl-N-isopropyl)6-chloropyra zinecarboxamide produced an additive blockade of AMPA-induced OT release, whereas the N-type Ca2+ channel-preferring antagonist omega-conotoxin GVIA had no effect. These findings suggest that an EAA, most likely glutamate, participates in the physiological regulation of OT release in the lactating rat via actions at an AMPA/kainate receptor subtype that gates Na+ and Ca2+.
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PMID:Stimulation of oxytocin release in the lactating rat by central excitatory amino acid mechanisms: evidence for specific involvement of R,S-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid-sensitive glutamate receptors. 769 46


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