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

Prenatal stress in rats usually results in behavioral and developmental changes in offspring. This experiment assessed body weight during the first three weeks postpartum and subsequent behavior of the offspring when tested as adults. Pregnant females allocated to the stress condition were exposed during the third week of pregnancy to either predictable (NOV1) or unpredictable (NOV2) psychological novelty stress. At this time, pregnant rats were also treated with various doses of oxytocin or vehicle solution. The exposure to unpredictable novelty stress during the third week of pregnancy resulted in pups which were significantly heavier at birth than either control animals or those which had received predictable exposure to the novelty stress. In contrast, oxytocin treatment appeared to lower body weight of offspring compared to control animals. This effect was observed right up until Day 21 postpartum for animals exposed to the larger dose (11.6 I.U.) of oxytocin. When tested as adults, NOV1 and NOV2 offspring were found to defecate more in the open field setting suggesting the they were more emotional than control animals. It was concluded that psychological stress during pregnancy has a subtle effect on development and subsequent effects on later emotionality of the offspring when tested as adults.
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PMID:Prenatal exposure to predictable and unpredictable novelty stress and oxytocin treatment affects offspring development and behavior in rats. 133 51

Increased knowledge on the mechanisms whereby corticotropin releasing hormone (CRH) and opioid peptides mediate the effects of stress has helped us to understand the relationship between stress and disturbed reproductive function. Increases of CRH and beta-endorphin in the hypothalamus in stressful situations inhibits the secretion of gonadotropins, oxytocin and vasopressin. This may lead to amenorrhea, which often is a consequence of intensive training or psychological stress, or it may disrupt parturition and lactation. There is a relationship between ovarian function and opioid peptides in the hypothalamus. Opioid peptides increase during puberty and fall at the menopause. Oestradiol and progesterone increase beta-endorphin concentrations in the luteal phase of the menstrual cycle, and this is followed by a rapid fall at menstruation. These changes may mediate symptoms typical of the premenstrual syndrome. Rather intensive exercise is required to increase plasma concentrations of beta-endorphin and corticotropin. During labour the amounts of beta-endorphin and corticotropin reach the values found in athletes during maximal exercise. The placenta produces increasing amounts of CRH towards the end of pregnancy which may help the mother and fetus to withstand the increased demands of labour. The placenta may thus be involved in the adaptation of the stress mechanism during pregnancy. CRH has also a paracrine function in different biological processes of the placenta and fetal membranes. It is possible to counteract the deleterious effects of stress on reproductive function by the administration of opiate antagonists. Induction of ovulation with naltrexone has been shown in patients with hypothalamic amenorrhea but the effect on fertility is not known.
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PMID:Corticotropin-releasing hormone and opioid peptides in reproduction and stress. 175 18

We studied the mechanism of normal lactation, especially the roles of prolactin (PRL) and oxytocin (OXT) in the initiation of lactation, the lactation in the women complicated with endocrinological disorders, and medical therapies for stimulation and suppression of lactation. The level of serum PRL increases as pregnancy progresses, and reaches to a peak on the day of delivery. Despite high PRL level, milk secretion does not appear during pregnancy, because the sex steroid hormones suppress binding of PRL to the receptor in the mammary gland. The initiation of milk secretion in puerperal women seems to be closely related to an increase in PRL levels induced by adequate suckling. In the mechanism of suckling-induced PRL increase, OXT from posterior pituitary seems to have an important role. Furthermore, the poor response of PRL to suckling was due to insufficient stimulation to the nipples by suckling because the size of nipples were relatively small in these mothers. The other mechanism involved in lactation is suckling-induced OXT secretion. OXT stimulates milk ejection. Anxiety or fear may inhibit the OXT release. We demonstrated that the number of pulsatile release of OXT by nursing was significantly decreased by the psychological stress induced by mental calculation. In the puerperal women with prolactinomas after surgery, the serum PRL level did not increase during pregnancy and milk secretion in puerperium was poor. In the puerperal women with diabetes mellitus, milk secretion was also poor. One of the causes may be related to the low PRL response to suckling stimuli. PRL stimulates milk yield in the mammary gland, but is not commercially available.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hormonal control of lactation]. 223 Apr 14

Oxytocin (OT), arginine-vasopressin (AVP), memory, and mood changes were measured in relation to the psychological stress of exposure to uncontrollable noise (UN), with the physical stress of exposure to the identical, but controllable, noise (CN) as a comparison. Four experiments were performed. In the first, UN but not CN resulted in OT increases in women but not in men; neither treatment altered plasma AVP. No significant changes were detected in the second study, but in the third women again showed an OT response to UN. In both the first and third study the OT response was found in only a proportion of the women exposed to UN. This result was analysed further in the fourth study, in which the stress-induced OT response occurred in high, but not in low, emotionality women. In the fourth, but not in the third, study there was an indication that OT increases may be associated with a general impairment of memory. There was no evidence to support an enhancement of negative memories after exposure to UN. Exposure to noise generally produced a worsening of mood, with no consistent differences between the UN and CN conditions. This is the first report of an OT response to psychological stress in human subjects.
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PMID:Psychological stress of exposure to uncontrollable noise increases plasma oxytocin in high emotionality women. 236 15

The effects of intravenous injections of naloxone (2 mg/kg), morphine (0.3 mg/kg) and saline vehicle on plasma concentrations of cortisol, prolactin, vasopressin and oxytocin were assessed in sheep (N = 10) when in their social groups (basal conditions) and during a period of isolation (psychological stress). Blood samples were collected by jugular venipuncture before and during the 60-min period following drug administration. Plasma hormone concentrations were determined by radioimmunoassay. Under basal conditions, cortisol levels were increased after naloxone (36-48%), but not after morphine or saline, and concentrations of prolactin, vasopressin and oxytocin did not change. Under stress conditions, (1) cortisol concentrations were elevated throughout the 60-min sampling period after naloxone or saline but for only 20 min after morphine; maximum increases observed were 161% (naloxone), 150% (saline) and 112% (morphine); (2) prolactin levels were raised after saline (85-129%) and morphine (55-61%) but were unchanged after naloxone; (3) vasopressin concentrations decreased transiently (43%) after saline but not following naloxone or morphine; and (4) oxytocin levels did not change after any treatment. These results indicate that endogenous and exogenous opioids modulate cortisol release in nonstressed sheep, and cortisol and prolactin secretion in sheep subjected to psychological stress. The nature of the anterior pituitary responses induced, together with the absence of a discernible effect on posterior pituitary function, suggest that the central opioid systems involved are similar in sheep and primates but different from those in the rat.
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PMID:Opioid influences on pituitary function in sheep under basal conditions and during psychological stress. 256 Feb 23

The aim of these experiments was to investigate the effects of psychological stress and oxytocin treatment on levels of norepinephrine, dopamine and serotonin in the hypothalamus, hippocampus, striatum, midbrain and brainstem of lactating females. Stress and oxytocin treatment were applied during the third trimester of pregnancy, and females examined on day 6 and day 21 postpartum. The results indicated that serotonin levels were significantly increased on day 6 following unpredictable novelty stress during pregnancy. Furthermore, a marked reduction in serotonin levels in the hypothalamus, hippocampus, midbrain and brainstem was observed as a result of oxytocin treatment on both Day 6 and Day 21 postpartum. These results are in stark contrast to those obtained for nulliparous females in a previous study and suggest an important distinction between nulliparous and lactating females with respect to the effects of psychological stress and oxytocin treatment on central monoamine levels.
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PMID:Psychological stress and oxytocin treatment during pregnancy affect central norepinephrine, dopamine and serotonin in lactating rats. 258 34

This study was designed to examine the effects of psychological stress and oxytocin treatment (5.8 or 11.6 IU/kg) on noradrenaline, dopamine and serotonin levels in the hypothalamus, hippocampus and brainstem. Results indicated that repeated exposure to the novelty stressor resulted in amine levels which did not significantly differ from those of control levels. In contrast, oxytocin treatment produced a significant elevation in serotonin levels in each of the three brain regions examined, while the effects for dopamine were confined to the hypothalamus. Furthermore, when oxytocin was administered immediately prior to unpredictable exposure to the novelty stressor, a significant increase in levels of noradrenaline in the hypothalamus and serotonin in the hippocampus and brainstem were observed. These results suggest that oxytocin may play an important role in modulating monoaminergic activity which is also apparent when the animal is exposed to a psychological stressor.
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PMID:Influence of exogenously administered oxytocin on central noradrenaline, dopamine and serotonin levels following psychological stress in nulliparous female rats (Rattus norvegicus). 274 63

Recent evidence suggests that oxytocin (OXT) potentiates corticotropin releasing factor-induced secretion of ACTH. The present study was therefore designed to investigate the possible role of oxytocin in the response to predictable and unpredictable novelty stress. The results clearly demonstrate that oxytocin produced a significant increase in corticosterone in all OXT treated animals. Repeated unpredictable exposure also produced a more substantial increase in corticosterone than predictable exposure to the same stressor. However, a significant interaction between stress and oxytocin was not obtained. It was concluded that whereas corticosterone is released in response to most types of stress, administration of oxytocin does not potentiate the corticosterone response to psychological stress.
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PMID:A possible role for oxytocin in the response to a psychological stressor. 374 16

Colchicine blockade of axonal transport from the paraventricular nucleus to the median eminence was used to indirectly infer hypothalamic ACTH secretagog release in awake rats. Median eminence contents of CRF, arginine vasopressin (AVP) and oxytocin (OT) were determined by RIA after insulin-induced hypoglycemia, restraint, and novelty. Insulin decreased circulating glucose concentrations and increased ACTH and corticosterone values. Median eminence CRF and AVP content declined but OT content did not. Both novelty and restraint stressors increased circulating ACTH and corticosterone concentrations. Secretagog measurements indicated decreases in OT content without concomitant decreases in either CRF or AVP with both stressors. These results indicate that: 1) colchicine blockade of axonal transport is useful in studying patterns of secretagog release in animals undergoing psychological stressors; 2) in contrast to physical stressors, OT appears to be a major component of the hypothalamic-pituitary-adrenal response to psychological stress; 3) the patterns of secretagog release differ with regards to physical and psychological stressors.
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PMID:Patterns of adrenocorticotropin secretagog release with hypoglycemia, novelty, and restraint after colchicine blockade of axonal transport. 767 13

Exposure to hostile conditions initiates the secretion of several hormones, including corticosterone/cortisol, catecholamines, prolactin, oxytocin, and renin, as part of the survival mechanism. Such conditions are often referred to as "stressors" and can be divided into three categories: external conditions resulting in pain or discomfort, internal homeostatic disturbances, and learned or associative responses to the perception of impending endangerment, pain, or discomfort ("psychological stress"). The hormones released in response to stressors often are referred to as "stress hormones" and their secretion is regulated by neural circuits impinging on hypothalamic neurons that are the final output toward the pituitary gland and the kidneys. This review discusses the forebrain circuits that mediate the neuroendocrine responses to stressors and emphasizes those neuroendocrine systems that have previously received little attention as stress-sensitive hormones: renin, oxytocin, and prolactin. Anxiolytic drugs of the benzodiazepine class and other drugs that affect catecholamine, GABAA, histamine, and serotonin receptors alter the neuroendocrine stress response. The effects of these drugs are discussed in relation to their effects on forebrain neural circuits that regulate stress hormone secretion. For psychological stressors such as conditioned fear, the neural circuits mediating neuroendocrine responses involve cortical activation of the basolateral amygdala, which in turn activates the central nucleus of the amygdala. The central amygdala then activates hypothalamic neurons directly, indirectly through the bed nucleus of the stria terminalis, and/or possibly via circuits involving brainstem serotonergic and catecholaminergic neurons. The renin response to psychological stress, in contrast to those of ACTH and prolactin, is not mediated by the bed nucleus of the stria terminalis and is not suppressed by benzodiazepine anxiolytics. Stressors that challenge cardiovascular homeostasis, such as hemorrhage, trigger a pattern of neuroendocrine responses that is similar to that observed in response to psychological stressors. These neuroendocrine responses are initiated by afferent signals from cardiovascular receptors which synapse in the medulla oblongata and are relayed either directly or indirectly to hypothalamic neurons controlling ACTH, prolactin, and oxytocin release. In contrast, forebrain pathways may not be essential for the renin response to hemorrhage. Thus current evidence indicates that although a diverse group of stressors initiate similar increases in ACTH, renin, prolactin, and oxytocin, the specific neural circuits and neurotransmitter systems involved in these responses differ for each neuroendocrine system and stressor category.
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PMID:Forebrain pathways mediating stress-induced hormone secretion. 988 35


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