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

By use of an immunofluorescence histochemical technique with a cross-species reactive antiserum to porcine neurophysin-II the precise localization of neurophysin in the pituitary gland and the hypothalamic area of the brain of the sheep has been determined. Neurophysin was confined to neurosecretory pathways originating from the supraoptic and paraventricular hypothalamic nuclei. The major pathway terminates in the neurohypophysis but in addition a second neurophysin-containing pathway proceeds in the external infundibular zone of the median eminence-pituitary stalk and is associated with the presence of vasopressin. In sheep affected with the hereditary degenerative disease known as natural scrapie, this supraoptico-paraventriculo-infundibular pathway is preserved and hypertrophied, while the major pathway to the posterior lobe of the pituitary degenerates. The supraoptic and paraventricular nuclei in the sheep comprise at least two distinct but morphologically similar neuronal populations affected differently by the natural scrapie genome, one undergoing dissolution by middle-age and one surviving and becoming hyperactive. This premature ageing is probably associated with a primary biochemical lesion affecting the rate of the axonal flow of neurosecretory vesicles and of their discharge at synaptic terminals. Possible metabolic and circulatory bases for such an anomaly are considered. The presence of neurophysin in the rostral and caudal adenohypophysis supports the view that vasopressin is acting directly as a trophic-hormone releasing factor, possibly for the quick release of adrenocorticotropic hormone and of growth hormone. The relation of neurophysin-rich aggregations in the neurohypophysis to Herring bodies and the turnover of neurosecretory material are discussed.
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PMID:Neurophysin in the brain and pituitary gland of normal and scrapie-affected sheep--I. Its localization in the hypothalamus and neurohypophysis with particular reference to a new hypothalamic neurosecretory pathway to the median eminence. 1137 May 13

Adrenomedullin (AM) is a potent vasodilator peptide, which is initially isolated from tissue of human pheochromocytoma. In addition to the effect on cardiovascular system, previous studies suggest that AM plays some roles as a neuropeptide in the brain. In the present study, we examined the effect of AM on in vitro adrenocorticotropic hormone (ACTH) secretion stimulated by corticotropin-releasing hormone (CRH), vasopressin (VP) or oxytocin (OT) in cultured rat corticotrophs and on the response of plasma ACTH, corticosterone (B) and OT to shaker stress in vivo. In contrast to the previous report, basal or CRH (10(-9) M)-stimulated ACTH secretion was not affected by coincubation with AM. Either of VP (10(-8) M) or OT (10(-8) M) significantly increased ACTH secretion in cultured rat anterior pituitary cells (156.7+/-24.9 in basal incubation vs. 267.8+/-15.0 in VP-stimulation, P<0.05, and 308.6+/-41.3 pg/ml in OT-stimulation, P<0.05). AM (10(-10) M) significantly inhibited OT-stimulated ACTH secretion. AM tended to inhibit VP-stimulated ACTH secretion, although the inhibitory effect was not statistically significant. Thus, it is likely that AM attenuates OT-stimulated ACTH secretion in corticotrophs. In vivo study, male Wistar rats were prepared with a guide cannula in the lateral ventricle and a catheter in femoral artery for blood sampling. AM (0.5, 1.0 microg in 5 microl) or normal saline (5 microl, control) was intracerebroventricularly (i.c.v.) injected in conscious rats. Shaker stress (110 cycles/min for 5 min) produced a significant increase of plasma ACTH (baseline: 106.4+/-48.6; vs. just after stress: 388.9+/-56.1 pg/ml, P<0.05) and B (baseline: 198.6+/-46.8 vs. 15 min after stress: 378.5+/-13.6 ng/ml, P<0.05) in the control group. Plasma OT tended to increase after stress, although the change was not significantly different (baseline: 29.8+/-6.5; just after stress: 65.6+/-18.2 pg/ml). I.c.v. injection of AM at 3 min before the stress did not significantly affect stress-induced changes of plasma ACTH, B and OT. These results suggest that AM has an inhibitory effect on OT-induced ACTH release in vitro and the inhibitory effect may be overwhelmed in ACTH and B response to shaker stress.
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PMID:Effects of adrenomedullin on adrenocorticotropic hormone (ACTH) release in pituitary cell cultures and on ACTH and oxytocin responses to shaker stress in conscious rat. 1174 58

Single stress induces long-lasting changes in the hypothalamo-pituitary--adrenal (HPA) axis of adult animals. Selective oxytocin (OXT) receptor antagonist was administrated into the cerebroventricle of male rats to test its influence on plasma adrenocorticotropic hormone (ACTH) responses induced by immobilization stress. The ACTH level is significantly higher than the control level (P<0.05) up to 6 days after single stress. Although the OXT antagonist did not change the plasma ACTH level at the end of single stress (P=0.59), the antagonist significantly decreased the ACTH concentration at the end of repeated (3 days) stress and 2 days after single stress (P<0.05) compared with controls. The results suggest that endogenous brain OXT enhances the long-lasting but not immediate HPA axis response to stress.
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PMID:Brain oxytocin augments stress-induced long-lasting plasma adrenocorticotropic hormone elevation in rats. 1188 Jan 97

The pituitary gland, the "master gland" of the body, is composed of endocrine cells, which secrete hormones essential for homeostasis. The gland consists of the adenohypophysis (anterior pituitary) and the neurohypophysis (posterior pituitary), two unique structures that differ anatomically and functionally. The neurohypophysis is innervated by nerve cells in the hypothalamus and forms the connection between it and the pituitary gland. The hypothalamus stimulates release and inhibition of pituitary hormones. The neurohypophysis secretes oxytocin and antidiuretic hormone. The adenohypophysis is composed of three structures: the pars distalis, the pars intermedia, and the pars tuberalis. The anterior pituitary (pars distalis) is responsible for the release of hormones that include growth hormone, prolactin, thyroid-stimulating hormone, follicle-stimulating hormone, luteinizing hormone, adrenocorticotropic hormone, and melanocyte-stimulating hormone. Disorders of the pituitary are predominately those of insufficient hormone release and may have profound effects on the neonate. The potential causes of and clinical symptomatology that may accompany pituitary hormone insufficiency in the neonatal period are explored.
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PMID:The pituitary gland: embryology, physiology, and pathophysiology. 1194 4

The primary aim of this study was to define the secretory dynamics of oxytocin and vasopressin in pituitary venous effluent from ambulatory horses during acute endotoxaemia, a stimulus that may release both hormones. Our secondary aim was to investigate the role of oxytocin in regulating adrenocorticotropic hormone (ACTH) secretion by comparing oxytocin, vasopressin, corticotropin-releasing hormone (CRH) and ACTH secretory profiles during endotoxaemia and by monitoring the ACTH response to oxytocin administration. Pituitary venous blood was collected nonsurgically continuously and divided into 1-min segments from eight follicular phase mares. Four mares were sampled for 30 min before and 3.5 h after receiving an i.v. infusion of bacterial endotoxin (TOX). Four control mares were sampled for 2.5 h without infusion of TOX. Another three follicular phase mares were given 5 U of oxytocin to replicate the peak response to TOX and pituitary blood collected every 1 min for 10 min before and 15 min after injection. Endotoxin raised the secretion rates of all hormones measured. All hormones were released episodically throughout the experiment, with TOX increasing the amplitude of peaks in each hormone. Peaks in oxytocin and vasopressin were coincident in each treated mare. Similarly, ACTH peaks were coincident with peaks of oxytocin and vasopressin in each treated mare, and with peaks of CRH in three mares. However, oxytocin administration did not affect ACTH secretion. We conclude that during endotoxaemia in horses: (i) oxytocin and vasopressin are secreted synchronously; (ii) oxytocin is unlikely to be acting as an ACTH secretagogue since inducing peak oxytocin concentrations observed during TOX does not raise ACTH; and therefore (iii) the close relationship between oxytocin and ACTH secretion is circumstantial and due to the fact that oxytocin secretion is concurrent with that of vasopressin, a proven ACTH secretagogue in horses.
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PMID:The effect of endotoxin administration on the secretory dynamics of oxytocin in follicular phase mares: relationship to stress axis hormones. 1212 90

Magnocellular vasopressinergic and oxytocinergic neurons of the hypothalamic supraoptic (SON) and paraventricular nuclei comprise the hypothalamic-neurohypophysial system, which is crucially involved in the regulation of body fluid and electrolyte homeostasis. However, still controversial is to what extent the same system influences the secretion of adrenocorticotropic hormone (ACTH) from the adenohypophysis. Therefore, we selectively stimulated magnocellular neurons of the SON of conscious male Wistar rats via retrodialysis. As expected, dialysis of the SON with hypertonic medium increased both the release of vasopressin within the SON and the secretion of vasopressin and oxytocin into the systemic blood circulation. This activation of the hypothalamic-neurohypophysial system was accompanied by a fivefold increase in plasma ACTH concentration. This effect was observed only if the tip of the microdialysis probe was within the SON. Intravenous infusion of the vasopressin V1 receptor antagonist d(CH2)5Tyr(Me)AVP significantly attenuated the effects of local osmotic stimulation of the SON on ACTH secretion. In contrast, administration of the same antagonist directly into the SON significantly enhanced the osmotically stimulated secretion of ACTH and corticosterone, primarily by delaying the restoration of the hormone secretion to prestimulation levels. We conclude from these findings that vasopressin from the hypothalamic-neurohypophysial system participates in the regulation of the hormonal stress response in a counterbalanced manner at the level of the SON and the adenohypophysis.
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PMID:Vasopressin from hypothalamic magnocellular neurons has opposite actions at the adenohypophysis and in the supraoptic nucleus on ACTH secretion. 1219 91

The RF-amide peptides (RFRPs), including prolactin (PRL)-releasing peptide-31 (PrRP-31) and RFRP-1, have been reported to stimulate stress hormone secretion by either direct pituitary or indirect hypothalamic actions. We examined the possible direct effects of these peptides on PRL and adrenocorticotropin (adrenocorticotropic hormone [ACTH]) release from dispersed anterior pituitary cells in culture and on PRL and ACTH secretion following intracerebroventricular (i.c.v.) administration in vivo. Neither peptide significantly altered PRL or ACTH release from cultured pituitary cells (male rat donors). Central administration of 1.0 and 3.0 nmol of PrRP-31, but only the higher dose of RFRP-1, significantly elevated serum corticosterone levels in conscious male rats. The effect of PrRP-31 was not blocked by pretreatment (i.v.) with the corticotropin-releasing hormone (CRH) antagonist, alpha-helical CRH 9-41; however, pretreatment of the animals (i.v.) with an antiserum to CRH significantly lowered the hypothalamic-pituitary- adrenal axis response to central administration of PrRP-31. On the other hand, the release of PRL was significantly elevated by 3.0 nmol of RFRP-1, but not PrRP-31, in similarly treated, conscious male rats. Pretreatment with the catecholamine synthesis inhibitor, alpha-methyl-para-tyrosine, prevented the stimulation of PRL secretion observed following central administration of RFRP-1. RFRP-1 similarly did not alter PRL secretion in rats pretreated with the dopamine, D(2) receptor blocker, domperidone. These results suggest that the RF-amide peptides are not true neuroendocrine regulators of stress hormone secretion in the rat but, instead, act centrally to alter the release of neuroendocrine factors that do act in the pituitary gland to control PRL and ACTH release. In the case of RFRP-1, stimulation of PRL secretion is potentially owing to an action of the peptide to inhibit dopamine release into the median eminence. The corticosterone secretion observed following central administration of PrRP-31 does not appear, based on our current results, to be solely owing to an action of the peptide on CRH-producing neurons but, instead, may be a result of the ability of PrRP-31 to increase as well the exposure of the corticotrophs in vivo to other ACTH secretagogues, such as oxytocin or vasopressin.
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PMID:Prolactin-releasing peptide and its homolog RFRP-1 act in hypothalamus but not in anterior pituitary gland to stimulate stress hormone secretion. 1266 69

Differential adaptive changes in serotonin2A [5-hydroxytryptamine (5-HT)2A] receptor signaling during treatment may be one mechanism involved in the latency of therapeutic improvement with antidepressants, such as fluoxetine. We examined the effects of fluoxetine (2, 3, 7, 21, or 42 days) on hypothalamic 5-HT2A receptor signaling. The hormone responses to an injection of the 5-HT2A receptor agonist (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-amino-propane HCl (DOI) were used as an index of hypothalamic 5-HT2A receptor function. Treatment with fluoxetine for 21 or 42 days produced diminished adrenocorticotropic hormone (ACTH) and oxytocin (but not corticosterone) responses to DOI injections (2.5 mg/kg i.p.; 15 min postinjection). Regulators of G protein signaling 4 and Galphaq protein levels in the hypothalamic paraventricular nucleus were not altered during fluoxetine treatment. Because previous studies indicate that treatment with fluoxetine for 21 days resulted in increased hormone responses to DOI when measured at 30 min after injection, we examined the effect of fluoxetine (21 days) on DOI-induced increase hormone levels at 15, 30, and 60 min after DOI injection. Fluoxetine decreased the oxytocin response at 15 but not at 30 min post-DOI injection, and potentiated the ACTH and corticosterone responses at 30 min post-DOI injection. For comparison, we examined the effect of fluoxetine on 5-HT2A receptor-mediated increase in phospholipase C (PLC) activity in the frontal cortex. 5-HT-stimulated, but not guanosine 5'-O-(3-thio)triphosphate-stimulated PLC activity was increased after 21 days of fluoxetine-treatment. Overall, these results indicate that chronic fluoxetine treatment can potentiate 5-HT2A receptor signaling in frontal cortex but differentially alters 5-HT2A receptor signaling in oxytocin-containing neurons and corticotropin-releasing factor-containing neurons in the paraventricular nucleus.
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PMID:Chronic fluoxetine differentially affects 5-hydroxytryptamine (2A) receptor signaling in frontal cortex, oxytocin- and corticotropin-releasing factor-containing neurons in rat paraventricular nucleus. 1272 28

An imbalance between serotonin-2A (5-HT2A) and 5-HT1A receptors may underlie several mood disorders. The present studies determined whether 5-HT2A receptors interact with 5-HT1A receptors in the rat hypothalamic paraventricular nucleus (PVN). The sensitivity of the hypothalamic 5-HT1A receptors was measured as oxytocin and adrenocorticotropic hormone (ACTH) responses to the 5-HT1A receptor agonist (+)-8-hydroxy-2-(di-n-propylamino) tetralin hydrobromide [(+)8-OH-DPAT] (40 microg/kg s.c.). The 5-HT(2A/2C) receptor agonist (-)DOI [(-)-1-(2,5-dimethoxy-4-iodophenyl)2-aminopropane HCl] (1 mg/kg s.c.) injected 2 h prior to (+)8-OH-DPAT significantly reduced the oxytocin and ACTH responses to (+)8-OH-DPAT, producing a heterologous desensitization of the 5-HT1A receptors. Microinjection of the 5-HT2A receptor antagonist MDL100,907 [(+)-alpha-(2,3-dimethoxyphenyl)-1-[2-(4-fluorophenylethyl)]-4-piperidinemethanol; 0, 10, or 20 nmol, 15 min prior to (-)DOI] into the PVN dose-dependently prevented the desensitization of 5-HT1A receptors induced by the 5-HT2A receptor agonist (-)DOI. Double-label immunocytochemistry revealed a high degree of colocalization of 5-HT1A and 5-HT2A receptors in the oxytocin and corticotropin-releasing factor neurons of the PVN. Thus, activation of 5-HT2A receptors in the PVN may directly induce a heterologous desensitization of 5-HT1A receptors within individual neuroendocrine cells. These findings may provide insight into the long-term adaptation of 5-HT1A receptor signaling after changes in function of 5-HT2A receptors; for example, during pharmacotherapy of mood disorders.
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PMID:Desensitization of 5-HT1A receptors by 5-HT2A receptors in neuroendocrine neurons in vivo. 1506 30

This study investigated the ability of prenatal exposure to cocaine to alter serotonin(2A) (5-HT(2A)) receptor function and paroxetine-induced desensitization of 5-HT(2A) receptor function in rat offspring. Following exposure to saline or (-)cocaine (15 mg/kg, s.c., b.i.d.), during gestational days 13-20, adult male offspring were treated with either saline or paroxetine (10 mg/kg/day, i.p. 14 days). Eighteen hours post-treatment, changes in the stimulation of oxytocin, adrenocorticotropic hormone (ACTH) and corticosterone by (-)4-iodo-2,5-dimethoxyphenylisopropylamine (DOI, 0.5 or 2.0 mg/kg, s.c.) and in 5-HT(2A) receptor densities were determined. Prenatal cocaine exposure did not alter 5-HT(2A) receptor-mediated neuroendocrine responses or 5-HT(2A) receptor densities. In contrast, paroxetine treatment reduced cortical 5-HT(2A) receptors (18-25%) and desensitized 5-HT(2A) receptor-mediated oxytocin responses in both offspring groups. Furthermore, in cocaine offspring, paroxetine produced an inhibition of 5-HT(2A) receptor-mediated increase in plasma ACTH levels and a greater attenuation of the oxytocin responses to (-)DOI. Paroxetine-induced reductions in body weight gain (-8.8%) were comparable in both offspring groups. These data, demonstrating that prenatal exposure to cocaine potentiates paroxetine-induced desensitization of 5-HT(2A) receptor function, may be clinically relevant with respect to treating mood disorders in adults exposed in utero to cocaine.
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PMID:Prenatal cocaine exposure potentiates paroxetine-induced desensitization of 5-HT2A receptor function in adult male rat offspring. 1508 91


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