Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Because of the enormous growth over the last three decades of research on the role of peptides in the brain, the need became apparent to determine the status of these compounds in terms of their current research interest. Since 1965, over a quarter of a million research papers have been published on peptides that have since been classified as neuroactive. The present study was undertaken to analyze systematically the yearly trends of research emphasis in neuroactive peptides as reflected by their individual frequency of publication by year, beginning in 1966. A computer analysis of the publication characteristics was carried out using the Medline data base in which the citation search was limited to the topic brain crossed with the topic mammal. One criterion for the inclusion of a given peptide in the analysis was a frequency of 25 or more citations following its discovery, as related to the mammalian brain. The 42 peptides that met this criterion were: adrenocorticotropic hormone, angiotensin II, atrial natriuretic factor, bombesin, bradykinin, calcitonin, calcitonin gene-related peptide, carnosine, beta-casomorphin, cholecystokinin, corticotropin-releasing factor, delta sleep-inducing peptide, dynorphin, beta-endorphin, Leu-enkephalin, Met-enkephalin, galanin, gastrin, glucagon, growth hormone, growth hormone-releasing factor, insulin, kyotorphin, beta-lipotropin, luteinizing hormone-releasing factor, melanocyte-stimulating hormone release inhibitory factor-1, alpha-melanocyte-stimulating hormone, motilin, neurokinin A, neurokinin B, neuropeptide Y, neurotensin, oxytocin, pituitary adenylate cyclase activating polypeptide, peptide HI, prolactin, secretin, somatostatin, substance P, thyroid-releasing hormone, vasopressin, and vasoactive intestinal peptide. An overall analysis of the 298,105 papers published on these 42 peptides since 1965 revealed that the research activity of 24,742, or 8.30%, of the studies, focused on their neuroactive properties. Taken as a whole, the research on neuroactive peptides reached a peak in 1986, as reflected by the total of 1793 papers published during that year. Although the level of publication has fluctuated between 1548 and 1774 research papers over the last 6 years, it is now clear that the trend in research on neuroactive peptides has reached an asymptote today that shows no sign of deviation. A temporal analysis year by year of individual publication profiles revealed three distinct trends: 1) peptides showed a slow development in research interest and did not exceed more than 15-30 publications per year; 2) peptides exhibited a steady increase in research activity over the years that continues today; and 3) peptides displayed an initial, often intense, research emphasis that inexplicably declined, in some cases precipitously, in the mid 1980s.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neuroactive peptides: unique phases in research on mammalian brain over three decades. 800 41

Glucocorticoid deficiency leads to elevated plasma vasopressin (AVP), while chronic endogenous hypercortisolism may inhibit osmotically stimulated AVP, suggesting that glucocorticoids may be feedback inhibitors of AVP secretion. We evaluated the effect of physiological increases in cortisol (65 mg/day iv) for 7 days on basal AVP and oxytocin (OT) in five conscious, male dogs. Cortisol increased from 1.3 +/- 0.1 to 5.0 +/- 0.8 micrograms/dl during infusion. Basal plasma AVP significantly decreased from 3.5 +/- 0.2 to 2.6 +/- 0.3 pg/ml during cortisol infusion. Plasma OT, osmolality, and sodium did not change while arterial pressure decreased (from 107 +/- 3 to 102 +/- 2 mmHg) on days 4 and 6. Increases in cortisol led to a physiologically significant, nonosmotic decrease in AVP. The effect was specific to AVP and independent of changes in arterial pressure. Glucocorticoid administration significantly decreased basal AVP within 24 h, which is comparable to the negative feedback control of adrenocorticotropic hormone. The inverse relationship between cortisol and AVP may account for the nonosmotic change in AVP in patients with disorders of glucocorticoid secretion.
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PMID:Physiological increases in cortisol inhibit basal vasopressin release in conscious dogs. 802 23

The effects of rat corticotropin-releasing factor (rCRF, 1.25 pmol/50 microliters/fetus), arginine vasopressin (AVP, 5 pmol/50 microliters/fetus) and oxytocin (OT, 12.5 pmol/50 microliters/fetus) alone or in association were investigated in 21-day-old rat fetuses injected intravenously through the umbilical vein. Blood samples were collected 15 and 30 min after injection for the determination of corticosterone concentration and the different plasma molecular adrenocorticotropic hormone (ACTH) forms isolated by chromatography on Sephadex G50 fine. All the plasma samples chromatographed 15 and 30 min after injection of the different peptides showed 3 different molecular ACTH forms: big ACTH (> 20,000 molecular weight), intermediate ACTH (= 13,000) and little ACTH (= 4,500). The injection of rCRF or AVP alone and rCRF in association with AVP or OT increased the concentrations of big ACTH 15 min and little ACTH 30 min after injection. The injection of OT alone or in association with AVP did not change the concentration of the 3 molecular ACTH forms 15 and 30 min after injection. The rise of big ACTH 15 min after injection was not associated with a significant increase in plasma corticosterone concentration, whereas the increase in little ACTH 30 min later enhanced plasma corticosterone concentration. Our results suggest that rCRF or AVP alone and rCRF in association with AVP or OT injected intravenously in the fetal rat produced a selective release of the molecular ACTH forms and the increase in the plasma corticosterone concentration occurred when the proportion of little ACTH which is the predominant ACTH form in the fetal rat was enhanced.
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PMID:Effects of corticotropin-releasing factor, arginine vasopressin and oxytocin on the polymorphism of plasma adrenocorticotropic hormone in the rat fetus in late pregnancy. 805 2

The relative abilities of the hypothalamic peptides corticotropin-releasing factor (CRF), arginine vasopressin (AVP), oxytocin (OT), and angiotensin II (ANG II) to stimulate adrenocorticotropic hormone (ACTH) secretion from cultured sheep anterior pituitary cells were studied. Incubation of cells with CRF, AVP, and OT, but not ANG II, was associated with increased ACTH secretion. CRF and AVP were equally effective in stimulating ACTH release at 0.1 nM, but larger doses of each resulted in distinctly different ACTH secretory patterns. The minimally effective dose of OT was 10 nM; greater doses of this peptide resulted in ACTH secretory responses similar to those measured after addition of AVP. Cotreatment with ANG II did not affect the ACTH-secretory response to CRF, AVP, or OT. These data confirm that AVP is a potent stimulus for ACTH secretion from sheep anterior pituitary in vitro and also show that CRF is effective in low concentrations in releasing ACTH. In contrast, the data do not support a regulatory role for ANG II in stimulating ACTH release directly from sheep corticotroph cells.
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PMID:Hypothalamic peptide regulation of ACTH secretion from sheep pituitary. 823 55

Various endocrine responses to 5-hydroxytryptamine (serotonin, 5-HT) agonists were used to assess serotonergic receptor function after chronic treatment with the antidepressants fluoxetine (10 mg/kg), a 5-HT uptake blocker and the norepinephrine uptake blocker desipramine (DMI, 5 mg/kg). Both were injected (i.p.) once a day for 21 days. DOI (5-HT1C/2 agonist, 0-5 mg/kg i.p.) and 6-chloro-2-[1-piperazinyl]-pyrazine (MK-212) (less selective, but predominantly a 5-HT1C agonist, 0-20 mg/kg i.p.) were administered 18 hr after the final antidepressant injection and 30 min before decapitation. Chronic treatment with both fluoxetine and DMI produced a potentiation in most hormone responses to the 5-HT agonists (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-amino-propane HCl (DOI) and MK-212, although there were several differences in individual hormone responses to the two 5-HT agonists. Fluoxetine and DMI potentiated the MK-212- and DOI-induced increase of plasma oxytocin levels and potentiated the effect of DOI on plasma adrenocorticotropic hormone (corticotropin) and prolactin levels. In contrast, the effect of the high dose of MK-212 on plasma prolactin concentration was reduced by both antidepressants. Only MK-212 increased vasopressin levels and this effect was potentiated by fluoxetine, but not by DMI. Fluoxetine also significantly increased the resting level of plasma vasopressin. DMI potentiated the effect of MK-212 on plasma renin concentration. Pretreatment with fluoxetine significantly increased (38%) the Bmax for the 5-HT1C/2 agonist sites ([125I]DOI) in the hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term treatment with the antidepressants fluoxetine and desipramine potentiates endocrine responses to the serotonin agonists 6-chloro-2-[1-piperazinyl]-pyrazine (MK-212) and (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI). 839 20

Physical, emotional and metabolic stressors activate the hypothalamo-pituitary-adrenal (HPA) axis via multiple neural pathways. Final hypothalamic coding of stressor-induced adrenocorticotropic hormone (ACTH) secretion is mediated by differential release of ACTH secretagogues. These include, but may not be limited to, corticotropin-releasing factor (CRF), arginine vasopressin, oxytocin and, possibly, adrenaline. Among these substances, CRF serves as the predominant regulatory factor of this axis because its presence is obligatory for the action of intrinsically weaker secretagogues. Because neural input-encoding qualities of individual stressors utilize, in part, stimulus-specific pathways, the effectiveness of glucocorticoid negative feedback in modulating ongoing and subsequent activity of the HPA axis is dependent upon the type of stressor and the nature of the neural pathways mediating the initial activity. Studies suggest that responses to physical stressors (for example, haemorrhage) are resistant to classical intermediate feedback, whereas those to emotional/cognitive stressors (such as a novel environment) are strongly susceptible to feedback. Overall functional characteristics of the HPA axis in adult organisms are at least partially a result of neonatal experience. In the adult differences in hypothalamic CRF mRNA levels, median eminence peptide content and pituitary responsiveness to stressors can be correlated with aspects of neonatal experience.
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PMID:Central and feedback regulation of hypothalamic corticotropin-releasing factor secretion. 849 Oct 95

It is well established that corticotropin-releasing hormone (CRH) is a principal neuropeptide which mediates the adrenocorticotropic hormone (ACTH) secretory response to interleukin (IL)-1 in the rat. It has recently been suggested that besides CRH, arginine vasopressin may also play a stimulatory role in IL-1 induced ACTH secretion. However, it remains to be elucidated whether other neuropeptides possessing an ACTH-releasing activity are involved in this neuroendocrine event. Therefore, in this study, we examined possible roles for oxytocin (OT) and cholecystokinin (CCK)-8 in the IL-1-induced ACTH response, utilizing the technique of immunoneutralization of these peptides. For comparison, we examined the effect of CRH immunoneutralization as well. Human recombinant IL-1 beta (50 ng) was given intracerebroventricularly (to the 3rd ventricle) to freely moving male rats 15 min after injecting specific antiserum against CRH, OT, or CCK-8, or normal rabbit serum (control) via the same route. As expected, anti-CRH antibody significantly suppressed the ACTH response to IL-1 beta. Interestingly, anti-OT antibody acted in the same manner, whereas anti-CCK-8 antibody did not. These results suggest that in addition to CRH and arginine vasopressin, OT may also play a significant role in mediating the IL-1 beta-induced ACTH secretion in the rat.
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PMID:Involvement of oxytocin and cholecystokinin-8 in interleukin-1 beta-induced adrenocorticotropin secretion in the rat. 852 Nov 44

Stimulation of gastric vagal afferents by systemic administration of cholecystokinin octapeptide (CCK) inhibits gastric motility, reduces food intake, and stimulates pituitary secretion of oxytocin and adrenocorticotropic hormone in rats. To characterize further the central neural circuits responsible for these effects, the present study used triple-labeling immunocytochemical methods to determine whether or not exogenous CCK activates cFos expression in catecholaminergic neurons in the caudal medulla that project to the paraventricular nucleus of the hypothalamus (PVN). To identify these neurons, the retrograde tracer fluorogold (FG) was iontophoresed into the PVN of anesthetized rats under stereotaxic guidance. After 2 weeks, rats were injected with CCK (100 micrograms/kg, i.p.) and then anesthetized and killed 1 hour later by perfusion fixation. Medullary sections were processed for triple immunocytochemical localization of cFos, retrogradely transported FG, and tyrosine hydroxylase (TH). In rats with FG injections centered in the PVN (n = 10), approximately 70% of the FG-labeled neurons in the caudal nucleus of the solitary tract (NST) and ventrolateral medulla (VLM) expressed cFos. Of these activated PVN-projecting neurons, approximately 78% in the NST and 89% in the VLM were catecholaminergic (TH positive). These results indicate that PVN-projecting catecholaminergic neurons within the caudal medulla are activated by peripheral administration of CCK, further implicating these ascending catecholaminergic pathways in the neuroendocrine, physiological, and behavioral effects produced by gastric vagal stimulation.
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PMID:Cholecystokinin activates catecholaminergic neurons in the caudal medulla that innervate the paraventricular nucleus of the hypothalamus in rats. 852 45

Immuno- and hybridization histochemical methods were used to examine a possible role for adrenocorticotropic hormone (ACTH) in regulating the expression of corticotropin-releasing peptides in rat hypothalamus. Densitometric assessments of relative levels of mRNAs encoding corticotropin releasing factor (CRF), arginine vasopressin (AVP) and oxytocin (OT) in the parvocellular division of the paraventricular nucleus (PVH) were carried out in intact, adrenalectomized (ADX) and hypophysectomized (HYPOX) animals. Both surgeries resulted in comparable increases in relative levels of CRF and AVP transcripts in the parvocellular PVH; no effects on OT mRNA in this compartment were evident. In a second experiment, ACTH or saline vehicle were administered systemically via osmotic minipump for seven days to rats submitted to both HYPOX and ADX surgeries. Lower replacement doses of ACTH reduced the number of detectable AVP-immunoreactive (AVP-ir) cells in the parvocellular PVH to 53% of that seen in vehicle-treated HYPOX/ADX controls; the number of CRF-IR cells was not significantly affected. Higher doses of ACTH resulted in counts of AVP- and CRF-IR neurons that were reduced to 32% and 70%, respectively, of control values. Staining patterns for the two peptides in the external lamina of the median eminence generally followed the cell count data. Neither densitometric nor combined immunohistochemical (for CRF-ir) and hybridization histochemical (for AVP mRNA) assays revealed any marked effect of ACTH on AVP mRNA expression in the parvocellular PVH of HYPOX/ADX rats. The results indicate that ACTH is capable of inhibiting corticotropin-releasing peptide, but not mRNA, expression in hypophysiotropic neurons. The mechanisms underlying these effects remain to be fully clarified.
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PMID:Evidence for short-loop feedback effects of ACTH on CRF and vasopressin expression in parvocellular neurosecretory neurons. 854 50

A 75-year-old female presented with a suprasellar granular cell tumor. Computed tomography (CT) revealed a high dense suprasellar mass with strong postcontrast enhancement. Magnetic resonance imaging showed a round suprasellar mass, which was hyperintense on the T1-weighted images with nonhomogeneous enhancement after the administration of gadolinium-diethylenetriaminepenta- acetic acid, and hypointense on the T2-weighted images. Cerebral angiography demonstrated no abnormal findings. The tumor was partially removed via a right frontotemporal craniotomy. The histological diagnosis was suprasellar granular cell tumor. Her postoperative course was uneventful other than mild and transient diabetes insipidus. She has remained asymptomatic without CT evidence of tumor regrowth for 20 months after the surgery. Immunohistochemical studies showed positive reaction for S-100 protein in the tumor cell nuclei, but no reaction for glial fibrillary acidic protein, neurofilament protein, Leu-7, oxytocin, beta-endorphin, adrenocorticotropic hormone, and vimentin. This case provides additional evidence for the astrocytic origin of suprasellar granular cell tumor.
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PMID:Suprasellar granular cell tumor. 874 Dec 54


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