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

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

The activity of protein carboxymethylase and the endogenous protein methyl acceptor capacity were examined in the posterior, intermediate, and anterior lobes of the pituitaries of homozygous Brattleboro rats with diabetes insipidus and in heterozygous Brattleboro and Long-Evans control rats. Protein carboxyl methylation is selectively altered in the posterior pituitary lobes of homozygous Brattleboro rats. Protein carboxymethylase activity is higher (+40%) and endogenous methyl acceptor protein capacity is lower (-80%) with respect to heterozygous Brattleboro and Long-Evans control rats. This latter change is correlated with decreased methylation of proteins of a molecular weight of approximately 11K daltons, is selective for the posterior pituitary lobe, since it does not occur in the intermediate and anterior lobes, and probably reflects the absence of vasopressin-associated neurophysin in homozygous Brattleboro rats. Our results support a physiological role of protein carboxyl methylation in the neurosecretory process in the posterior pituitary gland.
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PMID:High-protein carboxymethylase activity and low endogenous methyl acceptor proteins in posterior pituitary lobe of rats lacking neurophysin-vasopressin (Brattleboro rats). 686 19

A cell-by-cell analysis of the magnocellular elements in hypothalami of fifty Long-Evans (normal) and Brattleboro (diabetes insipidus) rats was done using the unlabeled antibody enzyme technique (PAP) with primary antisera directed against oxytocin (OXY), vasopressin (ADH), and the neurophysins. The magnocellular neurons of the hypothalamus were found in the supraoptic (SON), paraventricular (PVN), and anterior commissural (ACN) nuclei, a number of accessory nuclei, and as individual cells in the anterior hypothalamic area. SON was divided by the optic tract into the principal part and retrochiasmatic SON. In retrochiasmatic SON a majority of the cells contained vasopressin. Within the principal part of SON oxytocin-producing cells tended to be found rostrally and dorsally, while the vasopressin cells were more common caudally and ventrally. PVN was divided into three subnuclei, the medial, lateral, and posterior subnuclei, on the basis of cellular morphology and peptide content. The magnocellular cells of the medial and lateral PVN were closely packed together and nearly round, while those of posterior PVN were more separated and fusiform in shape with their long axis running in a medio-lateral direction. Medial PVN consisted primarily of oxytocin-producing cells, while lateral PVN was formed by a core of vasopressin-producing cells with a rim of oxytocin cells. Posterior PVN contained largely oxytocin-producing cells. Both ADH and OXY cells were found in the accessory nuclei. In the Long-Evans rat the SON had, on the average, 1443 OXY and 3236 ADH cells; the PVN had 1174 OXY and 976 ADH cells; and the accessory magnocellular groups in the hypothalamus (including the ACN) had 1286 OXY and 552 ADH cells. The Brattleboro strain animal had similar numbers of cells in these nuclei. (The cells which contain ADH in normal animals were identified in the Brattleboro rat as large, neurophysin-negative cells.) Thus, a large fraction of the magnocellular oxytocin- and vasopressin-producing cells in the rat were located outside of the PVN and SON. One accessory cell group in particular, ACN, had 616 OXY cells, or about 50% as many as PVN. In each nucleus the sum of the numbers of OXY and ADH cells was approximately the number of neurophysin cells.
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PMID:Immunohistochemical analysis of magnocellular elements in rat hypothalamus: distribution and numbers of cells containing neurophysin, oxytocin, and vasopressin. 701 60

Oxytocin administration in rat infused with hypotonic saline is associated with a saliuresis and altered renal water excretion. The role of vasopressin in determining the pattern of oxytocin-induced changes in urine flow was investigated in Long Evans and vasopressin-deficient Brattleboro rats, which exhibit contrasting diuretic and antidiuretic responses to oxytocin. Ethanol anaesthesia and water loading in Long Evans suppressed plasma vasopressin levels and was associated with an antidiuretic response to oxytocin. Vasopressin administration in the Brattleboro rat reversed the oxytocin-induced antidiuresis normally observed in vasopressin deficiency. These results taken with previous observations, have been interpreted as indicative that oxytocin acts as a weak agonist at the renal vasopressin receptor. When plasma vasopressin is suppressed or absent oxytocin acts as a weak antidiuretic agent, but in the presence of higher vasopressin levels a diuretic response to oxytocin is seen which follows displacement of vasopressin, the more potent antidiuretic agent, from the renal receptor.
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PMID:The influence of vasopressin on oxytocin-induced changes in urine flow in the male rat. 711 93

The possible role of microvesicles and vacuoles in the recapture of membrane after pituitary hormone release by exocytosis has been studied in homozygous Brattleboro rats. These mutant animals are unable to synthesize vasopressin and exhibit a steady state hypersecretion of oxytocin from the neural lobe as a result of the osmotic imbalance caused by their diabetes insipidus. This can be converted to a second steady state which approximates to the rate of secretion found in normal Long Evans rats by the administration of exogenous vasopressin daily for 30 days. In the Brattleboro rat, presumptive oxytocinergic nerve endings contain typical 160-170 nm diameter neurosecretory granules; other magnocellular nerve endings contain a population of smaller (approximately 100 nm diameter) dense-cored granules. The number of dense-cored granules was reduced in both types of nerve ending in the hypersecreting Brattleboro rats, but increased as a result of vasopressin treatment to levels which, for the classical neurosecretory granules, approximated that found in Long Evans rats. The microvesicle population of the nerve endings was essentially similar in quantitative terms in all the three groups (i.e. hypersecreting Brattleboro rats; vasopressin-treated Brattleboro rats and Long Evans controls). The number of vacuoles, on the other hand, was increased in nerve endings in the hypersecreting animals but reduced to levels found in Long Evans rats in the Brattleboro animals treated with vasopressin. Furthermore, the size of the vacuoles was comparable to the size of the dense-cored granules contained in the nerve endings. These changes in the vacuole population are exactly those that would be predicted for an organelle responsible for recapture of the granule membrane. We therefore conclude that membrane retrieval after exocytosis of neurosecretory granules in the neural lobe is achieved by vacuoles and that these organelles probably retrieve the membrane of the granule intact.
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PMID:Membrane retrieval by vacuoles after exocytosis in the neural lobe of Brattleboro rats. 712 29

Intracerebroventricularly (i.c.v.) administered angiotensin II (ANG II) at a dose of 100 ng caused a large increase in plasma oxytocin levels in Long Evans (LE) rats and in rats heterozygous for hypothalamic diabetes insipidus (HZ). In rats homozygous for diabetes insipidus (DI) even 100 fold higher doses of ANG II i.c.v. exerted only marginal effects on oxytocin release. The impaired responsiveness in DI rats was fully restored by prolonged treatment with a vasopressin (AVP) analogue. These data show that the decreased sensitivity of ANG II receptors in DI rats is due to the AVP defect and its metabolic consequences and can be reversed by AVP substitution.
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PMID:Angiotensin stimulates oxytocin release: imparied response in rats with genetic hypothalamic diabetes insipidus. 712 94

1. The present study investigates the nature and magnitude of the renal response to plasma levels of oxytocin which might be induced by salt loading. 2. Increased plasma osmolality induced by loading with NaCl is an effective stimulus for oxytocin release in the unanaesthetized male rat. Plasma oxytocin concentration was positively correlated (r = 0-.77) with plasma osmolality. Plasma oxytocin (muu./ml.) = 0.37 x (plasma osmolality (m-osmole/kg) -297). 3. In anaesthetized Long Evans rats intra-atrial administration of oxytocin at rates of 0.05 and 0.15 m-u./ml. produced plasma hormone concentrations (5 +/- 1 and 16 +/- 2 mum./ml. respectively) within the range induced by salt loading. 4. Oxytocin administration at 0.15 and 1.5 m-u./min in Long Evans rats produced dose-related increases in urine flow and Na+ and Cl- excretion. Renal responses to 0.05 m-u. oxytocin/min were equivocal. 5. Oxytocin administration at 0.15 m-u./min was ineffective in Brattleboro rats but 1.5 m-u./min led to increased Na+ and Cl- excretion and a reduction in urine flow. 6. Plasma oxytocin levels similar to those induced by severe dehydration or salt loading are effective in increasing renal Na+ and Cl- excretion and urine flow. These effects on water and electrolyte excretion appear to be independent of each other and both may be modified by the presence or absence of vasopressin. 7. This study provides no evidence for a major role for oxytocin in the day to day regulation of salt or water balance under conditions of normal hydration in the male rat.
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PMID:Release of oxytocin induced by salt loading and its influence on renal excretion in the male rat. 723 26

Brattleboro rats, homozygous for diabetes insipidus, and Long-Evans rats were anaesthetized with urethane, and antidromically identified neurons were recorded from the supraoptic nucleus. Phasically firing neurones were studied during repeated electrical stimulation of the neural stalk, whereby most supraoptic neurones, but not the recorded neurone, were activated antidromically. Such stimulation consistently modified the discharge pattern of phasic neurones in Long-Evans rats, but was relatively ineffective in Brattleboro rats. These results suggest that the effects of neural stalk stimulation on discharge patterns in Long-Evans rats may be substantially mediated by the evoked release of vasopressin or neurophysin.
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PMID:Effects of neural stalk stimulation on phasic discharge of supraoptic neurones in Brattleboro rats devoid of vasopressin. 726 20

Supraoptic neurosecretory neurons express a prominent N-methyl-D-aspartate receptor system. Recent in vitro evidence reveals that N-methyl-D-aspartate receptor activation dramatically alters the spontaneous discharge patterns of supraoptic neurons. In this study we evaluate whether N-methyl-D-aspartate receptors in vivo contribute to the development of characteristic phasic discharge patterns displayed by vasopressin-secreting neurons. Intravenous administration of ketamine hydrochloride, a non-competitive N-methyl-D-aspartate receptor antagonist, was used to examine whether N-methyl-D-aspartate receptor blockade influences patterned spontaneous discharge observed in supraoptic neurosecretory neurons. Extracellular recordings were obtained from identified hypothalamic supraoptic neurons in pentobarbital-anaesthetized Long-Evans rats. Systemic administration of ketamine (< or = 1.5 mg/kg) potently suppressed spontaneous phasic discharge in 16/19 putative vasopressin-secreting cells. The ketamine-induced blockade was dose dependent, fully reversible and was associated with the complete blockade of activity evoked by local pressure application of N-methyl-D-aspartate, but not the activity evoked by alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionate receptor agonists (6/6 cells). Ketamine had no detectable effect on threshold or shape of antidromic action potentials. By comparison, the activity in 9/10 continuously active neurons (putative oxytocin-secreting) was unaffected by administration of identical doses of ketamine. These data suggest that N-methyl-D-aspartate receptors play an important role in regulating the onset and maintenance of spontaneous phasic activity patterns displayed by rat supraoptic vasopressin neurons in vivo.
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PMID:N-methyl-D-aspartate receptor antagonist ketamine selectively attenuates spontaneous phasic activity of supraoptic vasopressin neurons in vivo. 751 67

1. Vasopressin-secreting neurones in the rat hypothalamic supraoptic nucleus display patterned spontaneous phasic activity, which is apparently maintained in vivo through yet unidentified neurotransmitter system(s). The present investigation used extracellular recording techniques in anaesthetized Long-Evans rats to evaluate whether the neurotransmitter mechanism underlying phasic firing is provided via a family of ionotropic glutamate receptors. 2. N-Methyl-D-aspartate (NMDA) reliably evoked bursts of activity in twenty-seven of twenty-eight phasic neurones. Amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA) and kainate also elicited pronounced excitations in twenty-one of twenty-one and and fourteen of fifteen phasic cells, respectively. 3. A rapid blockade of on-going phasic activity was consistently induced following brief applications of both NMDA and non-NMDA receptor antagonists; extended application of antagonists resulted in prolonged silent periods, during which phasic activity failed to recur for minutes. Neither saline nor a cholecystokinin receptor antagonist influenced cell firing. 4. In contrast to putative vasopressin cells, application of NMDA receptor ligands did not affect the spontaneous activity in most putative oxytocin-secreting neurones, whereas kainate and AMPA potently excited seven of nine and four of five putative oxytocin cells, respectively. 5. These results imply that the maintenance of spontaneous phasic discharges in vivo in supraoptic vasopressin-secreting neurones requires tonic synaptic activation involving both NMDA and non-NMDA glutamate receptors. In putative oxytocin-secreting neurones, spontaneous firing appears to be predominantly regulated by non-NMDA receptors. Glutamatergic innervations may be in a unique position to influence the genesis of patterned electrical activity in supraoptic vasopressin neurones.
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PMID:Regulation of spontaneous phasic firing of rat supraoptic vasopressin neurones in vivo by glutamate receptors. 754 68


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