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)

Messenger RNAs occur within the axons of magnocellular hypothalamic neurons known to secrete oxytocin and vasopressin. In Brattleboro rats, which have a genetic mutation that renders them incapable of vasopressin expression and secretion and thus causes diabetes insipidus, injection into the hypothalamus of purified mRNAs from normal rat hypothalami or of synthetic copies of the vasopressin mRNA leads to selective uptake, retrograde transport, and expression of vasopressin exclusively in the magnocellular neurons. Temporary reversal of their diabetes insipidus (for up to 5 days) can be observed within hours of the injection. Intra-axonal mRNAs may represent an additional category of chemical signals for neurons.
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PMID:Reversal of diabetes insipidus in Brattleboro rats: intrahypothalamic injection of vasopressin mRNA. 154 98

Degeneration of magnocellular nerve terminals in the neurohypophysis was induced by compressing the pituitary stalk of anesthetized rats for 30 s using a triangle-shaped wire. Immediately after stalk compression (SC), rats exhibited markedly increased water intake characteristic of diabetes insipidus, followed by a triphasic pattern of fluid intake. In SC rats, arginine vasopressin (AVP) and oxytocin (OT) contents of the neurointermediate lobe (NIL) of the pituitary gland were significantly reduced to approximately 2.5% and approximately 10% of sham-operated controls, respectively. In contrast, OT, but not AVP, content of the stalk-median eminence (SME) of SC rats was significantly increased. Histological examination of the pituitaries showed substantial degeneration of the neural lobe with very scarce AVP-neurophysin and OT-neurophysin immunoreactivity, while both the anterior and the intermediate lobes appeared to be intact. Plasma AVP and OT responses to infusion of hypertonic NaCl were significantly blunted in SC rats compared to sham-operated controls. However, two days after surgery the secretory patterns of LH in SC rats were similar to those in the controls. These results indicate that controlled compression of the pituitary stalk results in selective degeneration of the neural lobe without causing permanent ischemic damage to the anterior pituitary, and produces marked sustained functional deficits in pituitary AVP and OT secretion. Consequently, SC provides an alternative means to achieve selective neurolobectomy in rats.
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PMID:Functional neurolobectomy induced by controlled compression of the pituitary stalk. 157 81

Indirect immunofluorescence histochemistry was used to investigate the distribution and extent of co-localization of chemical messengers in magnocellular neurons of the supraoptic and paraventricular nuclei. In order to increase the number of neurons immunoreactive to the antisera used, experimental manipulations were employed. The homozygous Brattleboro (diabetes insipidus) rat was also investigated. In untreated rats, only vasopressin- and oxytocin-like immunoreactivities could be observed. Colchicine treatment alone resulted in appearance of galanin-, dynorphin-, cholecystokinin-, [Leu]enkephalin- and thyrotropin-releasing hormone-positive cells. In hypophysectomized rats, all these markers, except tyrosine hydroxylase, showed substantial further increases. In addition, peptide histidine-isoleucine-immunoreactive cell bodies could now be seen. After salt-loading alone, tyrosine hydroxylase-like immunoreactivity was markedly increased, whereas vasopressin- and oxytocin-like immunoreactivity were very weak or undetectable. When salt-loaded rats received colchicine, corticotropin-releasing factor- and peptide histidine-isoleucine-like immunoreactivity in addition increased, whereas galanin- and dynorphin-like immunoreactivity markedly decreased. The Brattleboro rats resembled untreated rats, except their lack of vasopressin-like immunoreactivity, the marked increase in tyrosine hydroxylase-like immunoreactivity, and smaller increase in galanin- and dynorphin-like immunoreactivity. Addition of colchicine to Brattleboro rats resulted in some distinct further changes in that dynorphin-like immunoreactivity decreased in some neurons and that [Leu]enkephalin-, corticotropin-releasing factor- and peptide histidine-isoleucine-like immunoreactivity increased substantially. Several similarities could be observed between the salt-loaded and Brattleboro rats, with or without colchicine. However, a marked difference in immunoreactive [Leu]enkephalin levels was observed with no difference in dynorphin-like immunoreactivity, and opposite changes in galanin-like immunoreactivity. The results confirm the traditional view that hypothalamic magnocellular neurons in the supraoptic and paraventricular nuclei contain two separate cell populations, characterized by vasopressin and oxytocin, respectively, and that they contain additional messenger molecules in specific patterns. Vasopressin-containing neurons primarily express tyrosine hydroxylase, galanin, dynorphin, [Leu]enkephalin and peptide histidine-isoleucine, and to a minor extent cholecystokinin and thyrotropin-releasing hormone. Oxytocin-containing neurons mainly have cholecystokinin and corticotropin-releasing factor, and to a minor extent galanin, dynorphin, [Leu]enkephalin and thyrotropin-releasing hormone. Furthermore, our results detail individual co-existence situations among these putative messenger molecules. Thus, magnocellular neurons respond in a differential way to various stimuli and they store multiple bioactive substances in specific combinations.
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PMID:Localization of chemical messengers in magnocellular neurons of the hypothalamic supraoptic and paraventricular nuclei: an immunohistochemical study using experimental manipulations. 170 Oct 38

Familial neurohypophyseal diabetes insipidus in humans is a rare disease transmitted as an autosomal dominant trait. Affected individuals have very low or undetectable levels of circulating vasopressin and suffer from polydipsia and polyuria. An obvious candidate gene for the disease is the vasopressin-neurophysin (AVP-NP) precursor gene on human chromosome 20. The 2 kb gene with three exons encodes a composite precursor protein consisting of the neuropeptide vasopressin and two associated proteins, neurophysin and a glycopeptide. Cloning and nucleotide sequence analysis of both alleles of the AVP-NP gene present in a Dutch ADNDI family reveals a point mutation in one allele of the affected family members. Comparison of the nucleotide sequences shows a G----T transversion within the neurophysin-encoding exon B. This missense mutation converts a highly conserved glycine (Gly17 of neurophysin) to a valine residue. RFLP analysis of six related family members indicates cosegregation of the mutant allele with the DI phenotype. The mutation is not present in 96 chromosomes of an unrelated control group. These data suggest that a single amino acid exchange within a highly conserved domain of the human vasopressin-associated neurophysin is the primary cause of one form of ADNDI.
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PMID:A missense mutation in the vasopressin-neurophysin precursor gene cosegregates with human autosomal dominant neurohypophyseal diabetes insipidus. 174 Jan 4

Light microscopic observations using Nomarski interference contrast optics or darkfield optics on unstained aldehyde-fixed vibratome sections of hypothalami from normal young adult male and female Long Evans rats and from vasopressin-deficient Brattleboro rats, revealed the presence of cells in the supraoptic, paraventricular and periventricular nuclei which possessed yellow birefringent inclusions of globular or filamentous appearance in their somata. These inclusions were morphologically distinct from the large lipid droplets present in vasopressinergic magnocellular neurons of diabetes insipidus mice. Small portions of the vibratome sections containing the birefringent cells were excised and prepared for correlative electron microscopy. This revealed that the birefringent inclusions represented electron-dense material within cisterns of endoplasmic reticulum in magnocellular neurons. Antibodies to oxytocin or oxytocin-associated neurophysin immunolabelled the intracisternal electron-dense material and neurosecretory granules in resin-embedded ultrathin sections. Antibodies to vasopressin or vasopressin-associated neurophysin, and a panel of lectins did not label the intracisternal material. Quantitation revealed a small increase in the numbers of birefringent cells in aged rats and in rats drinking saline for 3 days. Subcutaneous injection of oestradiol benzoate for 7 days prior to fixation caused a large increase. After cessation of oestradiol administration the numbers of birefringent cells decreased; observations on the remaining cells showed that the endoplasmic reticulum cisterns were frequently fused with the plasmalemma, resulting in direct release of neurosecretory material into the extracellular spaces.
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PMID:Peptide accretions in the endoplasmic reticulum of magnocellular neurosecretory neurons in normal and experimentally manipulated rats. 181 Sep 24

The status of the arginine vasopressin-neurophysin-II (AVP-NPII) gene was studied in three families with autosomal dominant neurohypophyseal diabetes insipidus (AD-NDI). Restriction fragments of genomic DNA containing AVP-NPII sequences from affected individuals were not detectably different in size from those of normal controls. Thus, these individuals with ADNDI do not have apparent large deletions, insertions, or rearrangements of an AVP-NPII allele. Four restriction fragment length polymorphisms were detected with a probe for the adjacent gene on chromosome 20, oxytocin-neurophysin-I (OT-NPI). Linkage studies in these three families between the restriction fragment length polymorphism haplotypes and ADNDI phenotype strongly suggest cosegregation. This indicates that the genetic locus for ADNDI maps within or near the AVP-NPII locus and suggests that a defective AVP-NPII allele may be the basis of ADNDI.
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PMID:Molecular analysis of autosomal dominant neurohypophyseal diabetes insipidus. 196 69

A 32 year old I P II G with preexisting diabetes insipidus was treated with 1-(3-mercaptopropionic acid)-8-d-arginine vasopressin (DDAVP) during pregnancy. An otherwise normal pregnancy was marked only with an excessive weight increase. A healthy girl was delivered by secondary cesarean section at term. Postoperative the mother developed a water intoxication accompanying oxytocin-infusion. During nursing the diabetes insipidus improved significantly whereby DDAVP doses could be reduced to 20-10 percent. We suppose an overreaction to endogene oxytocin with an antidiuretic effect.
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PMID:[Pregnancy in diabetes insipidus--a case report with review of the literature]. 222 Jan 71

The case of a 30-year-old pregnant patient suffering from panhypopituitarism is presented. Pregnancy induced by HMG/HCG had been uneventful. Induction of labor by PGE2 vaginal tablets and by intravenous oxytocin at 42 gestational weeks failed and the patient was operated. Following the operation severe exacerbation of her diabetes insipidus occurred. Fluid balance mechanism failed and electrolyte status deteriorated rapidly. The importance of pitressin in maintenance of fluid and electrolyte balance in panhypopituitaric patients in labor and surgical trauma is stressed.
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PMID:Pregnancy in panhypopituitarism. 235 98

A comparative quantitative analysis was carried out on identified supraoptic neurones of male and female Wistar and Long Evans rats under normal conditions and after chronic osmotic stimulation, and in homozygous Brattleboro rats suffering from diabetes insipidus. The neurones were identified by immunocytochemical or morphological means. Osmotic stimulation resulted in significant increases in the number and extent of direct neuronal appositions and in the number of presynaptic terminals contacting two neurosecretory cells simultaneously ("double" synapses). In the supraoptic nuclei of both sexes these increases were restricted to the oxytocin secreting neurones. In Brattleboro homozygous rats treated with vasopressin, the proportion of oxytocinergic neurones in apposition was not modified, but the number of appositions per soma profile decreased as did the incidence of "double" synapses. In nuclei of osmotically stimulated rats, increase in cell volume affected both types of neurosecretory cell and was accompanied by an increase of the absolute extent of glial coverage. However, the extent of glial coverage of the oxytocinergic neurones did not match the hypertrophy of the cells, resulting in a decrease in their relative glial coverage, compared to normal hydrated animals. The increased neuronal appositions, therefore, cannot result simply from a retraction of glial processes. The structural reorganization of the oxytocinergic system observed during chronic osmotic stimulation was as extensive as that observed at lactation. Moreover, the changes were as extensive in Wistar as in Brattleboro lactating rats, although the latter have an added osmotic stimulus. This implies that lactation and osmotic stimulation do not produce additive effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Osmotic stimulation causes structural plasticity of neurone-glia relationships of the oxytocin but not vasopressin secreting neurones in the hypothalamic supraoptic nucleus. 242 93

The nonapeptide vasopressin is synthetized as part of a longer common precursor polypeptide, together with its carrier protein neurophysin and a glycopeptide of unknown function. The gene for this common precursor has been isolated and sequenced and shown to comprise three exons encoding, respectively, the protein domains approximately corresponding to the N-terminal leader peptide and hormone, to most of the neurophysin, and to the glycopeptide. In the Brattleboro rat, the hereditary hypothalamic diabetes insipidus, characteristic of this strain, has been shown to be caused by a single nucleotide deletion in the vasopressin gene. This leads to the much reduced synthesis of a mutant vasopressin precursor, whose C terminus is quite unlike that in wild-type rats and which does not appear to be correctly processed in vivo.
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PMID:Biosynthesis of vasopressin. 243 69


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