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)

The vasopressin (AVP) innervation in the male rat brain is decreased in senescence. This decrease is particularly pronounced in brain regions where AVP fiber density is dependent on plasma levels of sex steroids. Since plasma testosterone levels decrease progressively with age in the rat, the possibility of restoring central AVP innervation by peripheral testosterone supplementation was investigated by giving senescent (33 months) Brown-Norway rats subcutaneous implants of either empty or testosterone-filled silastic tubes for the period of 1 month. Plasma testosterone levels of testosterone-treated animals were restored to values which did not differ from those of young animals. The results show that the age-related decline in AVP fiber density can indeed be reversed by testosterone supplementation. In contrast, oxytocin innervation, which was previously shown not to be testosterone-dependent, was not restored. These results show for the first time restoration of a specific innervation pattern in the senescent rat brain mediated by peripheral hormones and indicate that a considerable plasticity is retained in the aging central nervous system.
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PMID:Testosterone supplementation restores vasopressin innervation in the senescent rat brain. 306 84

Adult male rats spend a great amount of time investigating novel juveniles. In contrast, rats re-exposed to the same juvenile 30 min after the initial exposure display little investigatory behavior. If the re-exposure occurs 2 h later, the juvenile is thoroughly investigated. These results have been interpreted to mean that rats form a transient memory for a particular juvenile. In the present study, memory was enhanced when the initial exposure to the juvenile was followed by another exposure to the same juvenile (retroactive facilitation) and impaired when exposure to the original juvenile was followed by exposure to another juvenile (retroactive interference). Arginine vasopressin had retroactive facilitating effects on social memory and these effects were blocked by the vasopressor antagonist dPTyr(Me)AVP. Moreover, the antagonist had retroactive interfering effects, since it impaired the recognition of a familiar juvenile. Oxytocin shared the same inhibitory pattern of action. These results suggest that neurohypophyseal peptides may have a prepotent role in modulating the mnemonic processing of chemosensory information associated with social interactions.
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PMID:Modulation of social memory in male rats by neurohypophyseal peptides. 310 59

The distribution of vasopressin (AVP)-containing or oxytocin (OXT)-containing neurons in the rat hypothalamus which project to the posterior pituitary was revealed by the combination of retrograde tracing of horseradish peroxidase (HRP) and immunohistochemistry. The majority of magnocellular neurons labeled with HRP were located in some of the hypothalamic nuclei, including the supraoptic nucleus and paraventricular nucleus. Many of these neurons were also immunostained by anti-AVP or anti-OXT. On the other hand, some of the immunostained neurons were not labeled with HRP in the dorso-medial and the most caudal parts of the paraventricular nucleus. These data confirmed previous reports concerning the distribution of AVP- or OXT-neurons projecting to the posterior pituitary, as a more direct visualization of both the neuropeptides and the retrogradely transported HRP in the same tissue section was attained. In addition, some of the HRP-labeled perikarya which seemed to have direct contact with the ventricular lumen were occasionally seen; its functional significance is discussed.
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PMID:The distribution of vasopressin- or oxytocin-neurons projecting to the posterior pituitary as revealed by a combination of retrograde transport of horseradish peroxidase and immunohistochemistry. 313 51

In the present study we report the properties of vasopressin (VP) receptors in the anterior pituitary gland and show that the number of these receptors is markedly affected by adrenalectomy and hypothalamic lesions. VP-binding activity was assayed in particulate fractions of rat anterior pituitary glands using tritium-labeled arginine VP ([3H] AVP) as tracer. In the presence of Mg2+ the radioligand interacted with a single class of high affinity, low capacity binding sites. Magnesium ions modulated the affinity of the receptors but had no effect on binding capacity. Guanine nucleotides decreased the amount of tracer bound in a dose-dependent manner by increasing the dissociation constant (Kd) of the binding reaction by approximately 2-fold. Increasing the concentration of Mg2+ did not prevent this effect. Bilateral adrenalectomy (ADX) decreased pituitary AVP-binding activity: binding fell by 30% 4 h after surgery and declined further to 10% or less of control at 4 days. The decrease in binding was primarily due to a reduction in the number of receptors. Daily administration of corticosterone inhibited the reduction of binding activity at 4 days in a dose-dependent manner. Destruction of hypophyseotropic VP neurons by means of surgical lesioning of the hypothalamic paraventricular nucleus or the medial basal hypothalamus abolished the effect of ADX on pituitary AVP binding at 24 h but only attenuated the degree of receptor loss at 4 days. Furthermore, the lesions themselves caused a significant (approximately 30%) reduction in receptor number 4-7 days after hypothalamic surgery. Adrenalectomy reduced pituitary AVP-binding activity in homozygous (di/di) Brattleboro rats. The extent as well as the time course of the loss of receptor activity resembled that in normal rats. Rat anterior pituitary segments were exposed to synthetic CRF, AVP, or oxytocin (all 10(-7) M) for 4 h in vitro, and [3H] AVP-binding activity was subsequently determined. Both AVP and oxytocin reduced the amount of radioligand bound, while CRF had no effect. These observations allow the following conclusions: Magnesium ions and guanine nucleotides modulate the affinity of pituitary AVP receptors by different mechanisms and have no effect on binding capacity; Pituitary receptors for AVP are regulated by the amount of AVP released by paraventricular nucleus neurons as well as through a mechanism that requires the presence of corticosterone; Homozygous Brattleboro rats may respond to ADX by increased hypothalamic release of an endogenous ligand for pituitary AVP receptors.
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PMID:Pituitary binding of vasopressin is altered by experimental manipulations of the hypothalamo-pituitary-adrenocortical axis in normal as well as homozygous (di/di) Brattleboro rats. 316 22

Vasoactive intestinal polypeptide (VIP)ergic nerves innervate both the neurohypophysis and the hypothalamus. To test the hypothesis that VIP is a releasing factor for neurohypophyseal hormones, rats were given intracerebroventricular (icv) infusions of VIP in doses varying from 0.3 pmol/kg.min to 3 nmol/kg.min for 5 min (0.001-10 micrograms/rat). Serial blood samples were drawn from the vena cava for measurement of oxytocin (OT), vasopressin (AVP), and VIP by RIA. After the VIP infusions mean plasma OT and AVP levels rose in a dose-dependent manner; the rise was significant for both hormones at the dose of 300 pmol/kg.min. Peak levels after infusion of 3 nmol/kg.min were greater for OT than AVP [96.1 +/- 14.7 vs. 33.9 +/- 9 microU/ml (mean +/- SE); n = 6]. In addition, the concentration of plasma OT increased more promptly than that of AVP. Plasma OT was significantly raised over control values at 5 min, whereas plasma AVP was not increased until 15 min after the VIP infusion began. The concentration of VIP in peripheral plasma rose somewhat after icv infusions (maximum, 300 pmol/liter 30 min after 10 micrograms/rat), but the rise was only 5% of that observed after systemic infusions of equimolar doses of VIP (maximum, 6000 pmol/liter 5 min after 10 micrograms/rat). Peak plasma OT levels after administration of 3 nmol/kg.min VIP were significantly higher after icv than after systemic infusion of the same dose of VIP reported previously. Intravenous injection of 0.5 ml VIP antiserum with a binding capacity of VIP of 2.3 micrograms/ml before the icv administration of VIP (1 microgram/rat) did not prevent the VIP-induced rise in plasma OT and AVP. These observations suggest a central site of action for VIP in OT and AVP release, probably in the hypothalamus. The results are in harmony with the hypothesis that endogenous VIP is a physiological regulator of OT and AVP release in rats.
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PMID:Release of oxytocin and vasopressin by intracerebroventricular vasoactive intestinal polypeptide. 316 20

Because arginine vasotocin (AVT) activates male sexual behaviors in the rough-skinned newt (Taricha granulosa), quantitative autoradiography with radiolabelled arginine vasopressin (3H-AVP) was used to characterize putative AVT receptors in the telencephalon of this amphibian. Analyses were restricted to specific binding sites in the medial pallium, although dense binding also was observed in the dorsal pallium and amygdala pars lateralis. Binding of 3H-AVP to these sites was saturable, specific, reversible, of high affinity (Kd = 1 nM) and low capacity (57 fmol/mg protein). The rank order of potency of related peptides in inhibiting 3H-AVP binding was as follows: AVT greater than d(CH2)5[Tyr(Me)2]AVP (a mammalian pressor antagonist) greater than AVP, oxytocin, and [dPen1Tyr(Me)2]AVP (also a pressor antagonist) greater than mesotocin much greater than desGly(NH2)AVP, AVP fragment 4-9 and pressinoic acid. Thus, these binding sites appear to represent authentic central nervous system receptors for AVT. Furthermore, ligand specificity for the binding sites in this amphibian differ from that reported for AVP binding sites in rat brains. The AVT receptors in the medial pallium, dorsal pallium, and amygdala pars lateralis may represent site(s) of action where AVT elicits sexual behaviors in male T. granulosa.
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PMID:Autoradiographic characterization of binding sites labelled with vasopressin in the brain of a urodele amphibian. 317 42

The release of vasopressin (AVP) and oxytocin (OXT) within the septum was studied with the push-pull perfusion technique in 6 conscious, freely behaving male rats. Push-pull perfusion was performed via a chronically implanted cannula and samples collected for 3 consecutive 30-min periods. Stimulating electrodes were implanted in both the left and right paraventricular nuclei 4 days before the experiment. Bilateral electrical stimulation (10-s trains every 4 min) of the paraventricular nuclei during the second 30-min period resulted in a significant increase in the release of both AVP and OXT (128% and 159% of control values respectively); release returned to the pre-stimulation value during the final 30-min collection.
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PMID:Measurement of septal release of vasopressin and oxytocin by the push-pull technique following electrical stimulation of the paraventricular nucleus of rats. 317 31

A solution hybridization/RNase protection assay for the molar quantitation of vasopressin and oxytocin mRNAs, using synthetic complementary RNA probes, is described. This assay was optimized to permit the identification of vasopressin (AVP) mRNAs containing the frame-shift point deletion causing inheritable diabetes insipidus in the Brattleboro strain of rat. Examination of RNA from hypothalamic magnocellular tissue punches found that of the 86.1 x 10(-18) mol [86.1 attomoles (amol)] of AVP mRNA detected in the Brattleboro heterozygote paraventricular (PVN) nucleus, 5.2% could be shown to be mutant AVP mRNA (AVPd RNA). The percentage of AVPd RNA increased dramatically to 18.1% after 6 d of chronic intermittent salt-loading. Similar percentages and percentage increases of AVPd RNA were detected in the heterozygote supraoptic nucleus (SON). These values were contrasted with those found in parallel studies in both Long Evans and Brattleboro homozygotes, and compared with values for oxytocin (OT) mRNA in all 3 AVP rat genotypes. The results of continued osmotic regulation of the mutant AVP gene, the low native levels of AVPd RNA found in both the Brattleboro heterozygote and homozygote, and the magnitudes of AVPd expression change with chronic osmotic challenge were interpreted as indicating that (1) in the diploid rat genome, both AVP alleles are transcribed, (2) the osmotic regulation of the mutant AVP gene is normal, and (3) the low levels of AVPd mRNA are consistent with a shorter-than-control effective mRNA half-life.
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PMID:Differential expression of vasopressin alleles in the Brattleboro heterozygote. 319 79

1. Administration of 10 micrograms kg-1 of the long lasting potent kappa- and weaker mu-opioid agonist N-(cyclopropylmethyl)-19-isopentylnororvinol (M320) twice daily from day 20 of gestation prolonged the internal gestation period of the rat and retarded the development of the offspring in the perinatal period. 2. The capacities of myometrial, placental and cervical tissues to produce prostaglandin E2 (PGE2) were not affected by M320 treatment. 3. During the period in which parturition normally occurred in saline-treated rats, foetal pituitary levels of immunoreactive oxytocin (ir-OXY) but not immunoreactive arginine-vasopressin (ir-AVP) were greater in M320-compared to saline-treated animals. Following the completion of parturition, foetal pituitary ir-OXY and ir-AVP levels continued to rise in saline-treated rats, but fell dramatically in rats treated subacutely with M320. 4. These data indicate that subacute treatment with M320 may inhibit foetal oxytocin release at term. This foetal OXY release may be a stimulus for the initiation of labour.
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PMID:Studies of the effects of subacute treatment with N-(cyclopropylmethyl)-19-isopentylnororvinol (M320) on timing of parturition in the rat. 320 93

The methods of basolateral membrane isolation from rat kidney and 3H-AVP receptor assay using this basolateral membrane preparation were established. Then, the effects of analogues and drugs on AVP-receptor binding were studied. Specific 3H-AVP binding was inhibited by LVP, dDAVP and oxytocin in that order. Among the various agonistic or antagonistic drugs to AVP (fluoride, cyclophosphamide, mechlorethamine, chlorpropamide), only chlorpropamide inhibited 3H-AVP binding to the membrane. The Kd value calculated by Scatchard analysis was 1.30 +/- 0.28 nM (n = 4, M +/- SD), and it was increased to 2.69 +/- 0.32 nM (n = 5, M +/- SD) by adding 1 mM of chlorpropamide, while Bmax was unchanged. Our data show that 1 mM chlorpropamide decreases receptor affinity for AVP, and alters AVP-receptor binding in a competitive manner.
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PMID:[Effects of analogues and drugs on arginine vasopressin receptor binding in rat renal tubular basolateral membrane]. 321 97


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