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)

Using adjacent serial brain sections, a morphometric method has been developed for analysing the coexistence of the neurophysial hormones, vasopressin (VP) and oxytocin (OT), with their specific neurophysins (N). A significative correlation was found between the immunoreactive areas stained with (1) anti-VP and anti-N-VP sera, and between the immunoreactive areas detected with anti-OT and anti-N-OT antibodies. Besides, the immunoreactive areas stained with (1) anti-VP and anti-OT antibodies, (2) anti-N-OT and anti-VP antibodies, (3) anti-N-OT and anti-N-VP antibodies or (4) anti-OT and anti-N-VP antibodies were totally independent. A different method projecting the microscope images on a reference grid with a camera lucida permitted to quantify the coexistence of an ovine corticotropin-releasing factor-related-peptide (41-CRF) with OT in the paraventricular neurons of the Brattloro rat brain. In these animals, the same method applied after total hypophysectomy demonstrated that the neurons synthezising simultaneously 41-CRF and OT projected their axons to the neurohypophysis; the same operation increased the relative number of neurons containing 41-CRF only; it can be supposed that they originated the infundibular terminals.
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PMID:[The co-localization of neurohypophysis peptides and the corticotropin-releasing factor in the rat brain. Contribution of morphometric analyses]. 639 88

The localisation of corticoliberin producing neurones in the sheep hypothalamus was attempted with an antiserum directed against synthetic ovine CRF by the indirect immunofluorescence procedure. Synthetic ovine corticoliberin-immunoreactive fibres were detected, in order of decreasing importance, in the external median eminence, in the caudal neural lobe around capillaries, at the boundary of the neural and intermediate lobe, around the anterior commissure, in the paraventricular nuclei and in the posterior hypothalamus and midbrain, suggesting that synthetic ovine corticoliberin-related substances act not only on anterior pituitary tissue, but also on the intermediate lobe, on central neurones and on peripheral target organs. Two groups of cell bodies reacted to the anti-synthetic ovine corticoliberin antiserum. The first group was located in the paraventricular nuclei and consisted of 15-20 microns diameter cell bodies with a granular cytoplasm. The second group was located mainly in the dorsolateral caudal hypothalamus, and the cell bodies were smaller (10-15 microns) and had a smooth cytoplasm. No cell bodies were detected in the basal hypothalamus). Synthetic ovine corticoliberin-immunoreactive structures did not contain immunoreactive neurophysin. The synthetic ovine corticoliberin-immunoreaction in the paraventricular neurones was abolished by preincubating the antiserum with synthetic ovine corticoliberin but not with sauvagine or several other peptides. The immunoreaction in the posterior hypothalamic groups was abolished by preincubating the synthetic ovine corticoliberin antiserum with both synthetic ovine corticoliberin and sauvagine, but not with other peptides. The results suggest that the immunoreaction was specific for synthetic ovine corticoliberin in the paraventricular but not posterior hypothalamic region. The relative contribution of both areas to synthetic ovine corticoliberin-like peptides containing nerve terminals of the median eminence remains to be established.
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PMID:Corticoliberin-immunoreactive cell bodies localised in two distinct areas of the sheep hypothalamus. 641 Mar 5

The localization of CRF-41 related peptide was studied in the brain and posterior pituitary of the homozygous rats for the inherited diabetes insipidus (Brattleboro strain, DI) and of the Long-Evans rats (LE) as control. It was compared to the distribution of vasopressin (AVP), oxytocin (OXY) and OXY-neurophysin (N I). In both strains, CRF-41 was identified in two morphologically distinct systems: one was a hypothalamoneurohypophysial system simultaneously containing CRF-41, OXY and N I; the other was a hypothalamoinfundibular system carrying CRF-41 only. CRF containing neurons were located in the periventricular area of the anterior hypothalamus, in the retrochiasmatic part of the supraoptic nuclei (SON) and, for some of them, in the antechiasmatic part of SON. CRF immunostainings were enhanced by colchicine treatment in LE rats and by DDAVP therapy in DI rats.
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PMID:Comparative immunocytochemical localization of corticotropin releasing factor (CRF-41) and neurohypophysial peptides in the brain of Brattleboro and Long-Evans rats. 660 39

Immunohistochemical studies on cholecystokinin-like (CCK-ir) substances in colchicine-pretreated rats demonstrated that in addition to CCK-ir cells in the magnocellular portion of the paraventricular nucleus. CCK-ir cells are also present among the parvocellular neurons. Radioimmunoassay of CCK after paraventricular lesions indicate that most, if not all, of the CCK in the posterior pituitary and in the median eminence originates from the paraventricular nucleus. It appears that CCK-fibers, like other neuropeptidergic fibers from the paraventricular nucleus (vasopressin, oxytocin, TRH, CRF) enter the medial basal hypothalamus through a common gate--the lateral retrochiasmatic area--in traveling to the median eminence.
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PMID:Cholecystokinin in the hypothalamo-hypophyseal system. 672 68

By radioimmunoassay and immunocytochemical techniques, 14 neuropeptides have been measured and localized in the rat median eminence. Neuropeptides with inhibitory or stimulatory effects on the anterior pituitary hormones as well as posterior pituitary hormones are present in the median eminence in the highest concentrations of the central nervous system. All these peptides (LH-RH, TRH, somatostatin, CRF, vasopressin, oxytocin) are of preoptic or hypothalamic origin and they are transported to the median eminence by loop-like fiber systems through the lateral retrochiasmatic area. Within the median eminence, the pericapillary space constitutes the main common pathway. Three major transport routes--axons, vessels, liquor spaces--are separated from each others by only basement membranes, which allow free communications downwards to the pituitary but also backwards to the central nervous system.
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PMID:Neuropeptides in the median eminence: their sources and destinations. 681 29

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

Hypothalamic mechanisms of neurohormone regulation of endocrine pancreas in diabetes mellitus, adaptation to hypoxia and their combination were studied on Wistar rats. To evaluate the condition of supraoptic nucleus (SON) secretory function, paraventricular subnuclei (PVH) of hypothalamus and endocrine pancreas, we used radioimmunoassay, immunocytochemical, morphometrical and histochemical methods. Hyperglycemia, hypoinsulinemia, glucagon and somatostatin synthesis and secretion intensification in diabetes mellitus is accompanied by marked reorganization of hypothalamic neurohormones (CRF, vasopressin, oxytocin) secretion with corresponding signs of activity increase of synthesizing their hypothalamus nuclei and subnuclei and also ACTH, corticosterone, cortisol rise in blood. Adaptation to hypoxia caused hypoglycemia, activated insulin biosynthesis, changed glucagon and somatostatin synthesis and secretion. CRF concentration, corticosterone and cortisol, ACTH in blood was not changed, vasopressin concentration lowered, oxytocin in median eminence of hypothalamus increased to a higher degree than in diabetes. Adaptation to hypoxia corrected impaired hormone balance and state of Langerhans islets (beta-cells destruction process inhibition, insulin biosynthesis stimulation, glucagon and somatostatin secretion decrease) in diabetes mellitus, hypothalamic neurohormones participating in this process.
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PMID:[The vasopressin-, oxytocin- and corticoliberin-synthesizing structures of the hypothalamus in rats with diabetes mellitus under hypoxic exposures]. 790 84

Hyperglycemia, hypoinsulinemia, and an increase of glucagon and somatostatin concentration under diabetes mellitus are accompanied by intensification of secretion of hypothalamic neurohormones (CRF, vasopressin, oxytocin, somatostatin) with the corresponding signs of the increase in activity of hypothalamus nuclei and subnuclei secreting them as well as ACTH, corticosterone and cortisol rise in blood. Adaptation to hypoxia has caused hypoglycemia, activated insulin biosynthesis, changed glucagon and somatostatin synthesis and secretion. CRF corticosterone, cortisol and ACTH concentration in blood was not changed, vasopressin concentration lowered, somatostatin and oxytocin amount (in hypothalamus) increased to a higher degree than under diabetes. Adaptation to hypoxia corrected impaired hormone balance and state of Langerhans islets (beta-cells destruction process inhibition, insulin biosynthesis stimulation, glucagon and somatostatin secretion decrease) under diabetes mellitus, hypothalamus neurohormones participating in this process.
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PMID:[Hypothalamic mechanisms of neurohormone regulation of the endocrine part of the pancreas]. 790 82

Present knowledge allows the identification of some features of the initiation of human parturition. Progesterone reduces myometrial sensitivity to labour-inducing agents. It suppresses gap junction formation and facilitates beta-adrenergic receptor expression by the myometrium which, in turn, exerts a positive feedback by enhancing beta-adrenergic-induced increases in placental progesterone production. Inhibition of gestagen action does not result in immediate initiation of labor but sensitises myometrial cells to contraction-inducing agents. Estrogens, in contrast, enable the myometrium to prepare for parturition by inducing oxytocin receptors and this seems to be the first step towards parturition. Coordinated myometrial contractions are facilitated by the increased gap junctions due to the estrogen drive. Absence of estrogen will result in failed parturition. The myometrium seems to be sensitised to oxytocin by placental CRF. Myometrial CRF receptors increase their avidity for CRF with ongoing pregnancy. Oxytocin evokes a variety of auto- and paracrine events which culminate in increased free intracellular calcium and the consequent contractions. In this cascade, prostaglandins can be identified as positive feedback agents, as they further enhance estrogen-induced expression of oxytocin receptors. Another second messenger of oxytocin action are the inositol phosphates which can further increase free intracellular calcium concentrations. Finally, endothelin-1, derived from endometrium and decidua, under oxytocin control, may serve as a myometrial contractor following delivery when oxytocin concentrations decline but when a strong myometrial contraction is needed to prevent large blood loss during and after placenta expulsion.
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PMID:Placental progesterone, prostaglandins and mechanisms leading to initiation of parturition in the human. 799 41

To investigate functional and chemical properties of anatomically characterized corticotropin-releasing factor-41 (CRF-41) producing neurons in vitro, hypothalamic slices of 6-day-old rats were maintained in culture for up to 6 weeks using a modified roller culture technique. This technique yields thick (100 microns) slices that contained an average of 300-400 CRF-41-immunostained neurons. The majority of CRF-41-positive cells were of small size (12-15 microns in diameter), and contained CRF-41-labeled dense core vesicles of 100 nm diameter as detected by electron microscopic postembedding immunocytochemistry. These cells represented the only CRF-41-positive cell population in the culture. Light microscope double immunolabelling of colchicine-treated cultures kept in a serum-containing media (SCM) indicated that about 60% of these CRF-41-positive neurons contains detectable levels of vasopressin-associated neurophysin (VP-NP). Culturing slices in serum-free, chemically defined media (SFM) resulted in an increased VP-NP immunostaining: parvicellular neurons labeled for both CRF-41 and VP-NP could be detected without colchicine treatment, and practically all CRF-41-positive neurons expressed VP-NP immunoreactivity. At the electron microscopic level there was a significant increase in VP-NP labeling density in the dense core vesicle compartment of CRF-41-positive varicosities. Adding dexamethasone (10 nM) to the SFM restored the staining pattern originally observed in SCM. Hence, the increased VP-NP and CRF-41 immunostaining after culturing CRF-41 neurons in SFM is most likely due to the absence of inhibitory glucocorticoids. The capacity of cultured paraventricular cells to release CRF-41 was assessed using an immunoassay. Unstimulated (basal) secretion of CRF-41 was not altered by five successive samplings at 2-hour intervals and stimulation of the same culture with 56 mmol K+ significantly increased (2-3 times) the CRF-41 content in the medium. The presence of dexamethasone (10 nM) in SFM induced a 6-fold reduction of K(+)-stimulated CRF-41 release and a 5 times reduction in tissue content in relation to cultures maintained in SFM without dexamethasone. In summary, we have demonstrated that cultured CRF-41 cells display morphological and biochemical features, as well as responsiveness to glucocorticoids, that is reminiscent to the situation in vivo. Thus, the model is well suited for studies of hypophysiotrophic CRF-41 cell functions.
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PMID:A tissue culture model of the hypophysiotrophic CRF producing neuronal system. 836 34


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