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)

In several models of salt appetite in the rat, stimulated NaCl intake can be severely blunted by treatments associated with pituitary release of oxytocin (OT). Central administration of the potent dipsogen angiotensin II (ANG II) is known to elicit a limited salt appetite as well as thirst, but it has also been reported to stimulate pituitary OT secretion. These results suggest the possibility that the expression of ANG II-induced salt appetite in rats may be inhibited by a simultaneous central release of OT in response to this stimulus. To investigate this possibility, rats were given intracerebroventricular injections of OT-receptor antagonists before administration of 5 ng ANG II intracerebroventricularly in a 1-h two-bottle (water and 0.3 M NaCl) drinking test. This pretreatment resulted in a three- to fourfold potentiation of ANG II-induced saline ingestion, which was most prominent during the first 15 min of the test. OT-receptor antagonism did not, however, interfere with the dipsogenic properties of ANG II, nor did it stimulate saline ingestion alone in the absence of ANG II. Immunocytochemical studies demonstrated that central administration of ANG II at this dose caused pronounced c-fos expression in hypothalamic magnocellular OT and vasopressin neurons and also in OT neurons in parvocellular subdivisions of the paraventricular nucleus. These results therefore demonstrate that central administration of small doses of ANG II activates both magnocellular and parvocellular OT neurons in rats and indicate that some of the activated central OT pathway(s) may mediate an inhibitory effect that limits the salt ingestion induced by this treatment.
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PMID:Central oxytocin inhibition of angiotensin-induced salt appetite in rats. 133 19

Systemic administration of cholecystokinin (CCK) decreases gastric motility and stimulates pituitary secretion of oxytocin (OT). Although peripheral OT does not affect gastric function, increasing evidence suggests that central OT secretion acting within the dorsal vagal complex (DVC) can alter gastric motility. To evaluate whether systemically administered CCK is capable of activating oxytocinergic neurons projecting to the DVC, we utilized fluorogold retrograde labeling from the DVC in combination with c-fos and OT immunocytochemical staining to quantitatively analyze paraventricular nucleus (PVN) neurons of rats following injection of CCK at a dose known to cause maximal pituitary OT secretion (100 micrograms/kg i.p.). Our results showed that 2320 +/- 63 PVN neurons were retrogradely labeled from the DVC; 146 +/- 21 (6.3%) of these contained OT, and these cells were predominantly located in the medial parvocellular subdivision of the PVN. Of all retrogradely labeled cells, 671 +/- 112 (28.9%) expressed c-fos after CCK stimulation, and 68 +/- 14 of these (10.1%) contained OT. Approximately 50% of the OT-containing neurons retrogradely labeled from the DVC stained positively for c-fos. Many magnocellular OT neurons in the PVN that were not retrogradely labeled from the DVC also expressed c-fos after CCK stimulation. These results demonstrate that parvocellular OT neurons projecting to the DVC are co-activated along with magnocellular OT neurons projecting to the pituitary following administration of a large dose of CCK, and lend support to a possible functional role for OT as a central neurotransmitter that modulates vagal efferent traffic to the gastrointestinal tract.
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PMID:Cholecystokinin induces c-fos expression in hypothalamic oxytocinergic neurons projecting to the dorsal vagal complex. 137 8

Double immunostaining for c-fos and oxytocin (OXY) was used to study the topography and time course of the metabolic activation of the hypothalamic oxytocinergic system upon osmotic stress in the male rat. Animals injected i.p. with hypertonic saline expressed c-fos-like immunoreactivity (FLI) in the paraventricular (PVN), periventricular (PEV) and supraoptic (SON) hypothalamic nuclei, and in the preoptic and retrochiasmatic regions, as early as 30 min after stimulation and up to 6 h, while these areas were mostly devoid of staining in isotonic saline-injected animals. The activation of the oxytocinergic system peaked at 30 min and declined at different rates in the PVN and in the SON after 90 min. The maximal percentage of OXY neurons expressing FLI upon osmotic stress was about 80% in the SON, PEV and LSN, 60% in the PVN and 50% in the medial preoptic area. Activated OXY neurons were found in both the magnocellular and parvocellular divisions of the system. These data show that OXY nuclei in the rat hypothalamus are differentially activated by osmotic stress. They also suggest a role of OXY in the central as well as in the humoral response to changes in plasma osmolarity.
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PMID:Expression of c-fos protein by immunohistochemically identified oxytocin neurons in the rat hypothalamus upon osmotic stimulation. 139 70

Immunoreactivity to Fos protein (Fos-IR) was detected in rat hypothalamic neurons within 1 h of onset of hemorrhage by withdrawing 4-5 ml of blood, which lowered the arterial blood pressure to 50-70 mm Hg. About 70% of vasopressin (AVP)-containing neurons in the supraoptic nucleus (SON) and 20% in the paraventricular nucleus (PVN) expressed Fos-IR. In contrast, 5% of oxytocin (OXY)-containing neurons in the SON and < 1% in PVN were Fos-IR. Intravenous infusion of the vasodilating agent, nitroprusside, which lowered the blood pressure to levels comparable to that attained by hemorrhage, induced Fos-IR in greater than 65% of AVP-containing neurons in the SON, while relatively few AVP neurons in the PVN were Fos positive. These results suggest that hemorrhage or hypotension preferentially induces c-fos expression in supraoptic AVP-containing neurons.
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PMID:Hypotension preferentially induces c-fos immunoreactivity in supraoptic vasopressin neurons. 145 16

PRL secretion is regulated by an endogenous stimulatory rhythm of PRL-releasing factors within the hypothalamus. The endogenous rhythm has a bimodal periodicity with a nocturnal component which peaks at approximately 0300 h and a diurnal component that peaks at approximately 1700 h. Several PRL-releasing factors are known to be involved in this rhythm. Among these are oxytocin (OT), vasoactive intestinal peptide, and serotonin. We have proposed that OT is the neurohormone that stimulates PRL release from the lactotroph. In this study, we examined the activity of OTergic neurons in the paraventricular nucleus using the expression of the protooncogene c-fos (Fos) as a marker of neuronal activity. Ovariectomized rats were killed at either 0300, 1200, or 1700 h and brains quickly fixed by perfusion with 2.5% acrolein in 4% paraformaldehyde. Brains were blocked and processed for OT/Fos immunohistochemistry. Rats killed at 0300 and 1700 h had significantly greater proportion of Fos expressing OTergic neurons than control rats (1200 h). Percent of Fos-positive OTergic neurons were 2- and 1.5-fold greater at 0300 and 1700 h than 1200 h, respectively. The majority of these neurons were located in the medial parvocellular paraventricular nucleus and periventricular area. In another experiment, groups of OVX rats were killed every 2 h over a 24-h period and OT extracted from their anterior and posterior pituitaries. OT was present in the anterior pituitary in a bimodal rhythm. OT concentrations were greatest at approximately 0400 h and slowly declined to baseline by 1000 h. Another peak of OT was present in the anterior pituitary at approximately 2000 h and quickly declined to baseline by 2400 h. This rhythm of OT was not reflected in either the posterior pituitary or trunk blood. These data suggest that activity of a specific population of OTergic neurons of the paraventricular nucleus is rhythmic. The periodicity of these neurons mirrors that of the endogenous stimulatory rhythm. Furthermore, the anatomical location of these neurons suggests that they may project to the median eminence. Indeed, this heightened activity is reflected in a bimodal rhythm of OT in the anterior pituitary. Taken together, the data presented here provide compelling support for the role of OT as the neurohormone in the mechanism of the endogenous stimulatory rhythm.
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PMID:Activity of oxytocinergic neurons in the paraventricular nucleus mirrors the periodicity of the endogenous stimulatory rhythm regulating prolactin secretion. 172 95

Using immunofluorescence histochemistry, the paraventricular and supraoptic hypothalamic nuclei of normal control and hypophysectomized rats were studied in double labelling experiments with antibodies against the protein c-fos (Fos) and against vasopressin or oxytocin in order to characterize the activated neurons chemically. Normal controls showed no expression of Fos, whereas in hypophysectomized animals an intense induction of Fos-like immunoreactivity (-LI) was observed 12 h and 24 h post hypophysectomy but not beyond this survival time. Both vasopressinergic and oxytocinergic magnocellular neurons were labelled with Fos-LI. Thus Fos-LI can be induced in magnocellular hypothalamic neurons by injury, suggesting that this protein may be involved in adaptive mechanisms following axotomy.
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PMID:Transient induction of c-fos in rat magnocellular hypothalamic neurons after hypophysectomy. 181 Apr 61

1. The expression of c-fos mRNA in the rat hypothalamus was examined by in situ hybridization following systemic administration of cholecystokinin (CCK), a procedure known to activate magnocellular oxytocin neurons but not magnocellular vasopressin neurones. 2. Conscious male rats were given a single I.P. injection of 50 micrograms/kg CCK, c-fos mRNA signal was apparent in the supraoptic and paraventricular nuclei in rats killed 10 min after injection but not in uninjected or saline-(vehicle) injected rats. The density of c-fos mRNA at both sites was further elevated in rats killed 30 min or 60 min following injection, and was absent in rats killed 4 h after injection. 3. In the paraventricular nucleus the most dense expression of c-fos mRNA following CCK administration was in the medial, mainly parvocellular portion of the nucleus, in an area corresponding to the distribution of corticotrophin-releasing factor mRNA determined by in situ hybridization in adjacent sections. 4. The I.P. injection of CCK increased plasma oxytocin concentrations, measured by specific radioimmunoassay from 13 +/- 5 pg/ml in control rats to 107 +/- 9 pg/ml in the rats killed 10 min after injection, a similar response to that observed previously in urethane-anaesthetized rats. 5. In each of six urethane-anaesthetized rats, recordings were made from single neurones in the supraoptic nucleus, identified antidronomically as projecting to the posterior pituitary and identified electrophysiologically as putative oxytocin neurones. Following I.P. injection of 50 micrograms/kg CCK, the neurones increased their firing rate by a mean of 1.3 +/- 0.2 spikes/s averaged over the 10 min following injection. 6. From the appearance of c-fos mRNA in supraoptic neurones following CCK administration we conclude that this message is expressed in magnocellular oxytocin neurones, since vasopressin neuronal activity and vasopressin release is known to be unaffected by this stimulus, and since the supraoptic nucleus contains essentially only oxytocin neurones and vasopressin neurones. 7. We conclude that c-fos mRNA expression can be induced in supraoptic oxytocin neurones following brief and modest episodes of electrical activation, suggesting that c-fos may be involved in the gene regulation of these neurones under physiological conditions.
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PMID:Electrical activation and c-fos mRNA expression in rat neurosecretory neurones after systemic administration of cholecystokinin. 182 61

In order to evaluate the responses to osmotic stress of oxytocinergic neurons in vivo, we have studied oxytocin (OXY) and c-fos protein expression in the brain by means of double-immunostaining. C-fos immunoreactivity was detected in a subset of OXY neurons, as well as in other neurons non-immunoreactive for OXY, as early as 90 min after intraperitoneal injection of a hypertonic saline solution. C-fos expression was found in approx. 70% of OXY-immunoreactive neurons in the supraoptic (SON), lateral subcommisural (LSN) and paraventricular (PVN) nuclei, and not in OXY neurons in other hypothalamic areas. The expression of c-fos may be used as a means to map the circuitry by which osmotic stimulation activates OXY-containing neurons, and thus provide further insights into the functions with which OXY may be associated.
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PMID:Oxytocin neurons in the rat hypothalamus exhibit c-fos immunoreactivity upon osmotic stress. 212 73

Arginine vasopressin is a neuropeptide that has been shown to modulate functional ethanol tolerance and memory processes. These actions of vasopressin in the CNS have been shown by us and others to be mediated by V1 receptors. Intracerebroventricular injection of vasopressin in mice resulted in a substantial increase in mRNA for the proto-oncogene c-fos in septum and hippocampus, but no increase in cerebral cortex. A V1-selective agonist also increased septal c-fos mRNA levels, while a V2-selective agonist was less effective. Similarly, the response to vasopressin was more effectively blocked by a V1- than a V2-selective antagonist. These results indicate that vasopressin acts specifically at V1 receptors in mouse septum and hippocampus to increase c-fos mRNA. The vasopressin metabolite, AVP(4-9), also increased c-fos mRNA levels in septum and hippocampus, while the response to oxytocin, which has different effects from vasopressin on memory and tolerance, was greater in hippocampus than in septum. Nerve growth factor, in contrast to the other peptides, had a more pronounced effect on c-fos mRNA levels in cerebral cortex than in the other brain areas. Increased c-fos expression has been hypothesized to play a role in neuroadaptation, and these results suggest that modulation of septal c-fos expression could be important for vasopressin effects on ethanol tolerance and/or memory.
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PMID:Arginine vasopressin induces the expression of c-fos in the mouse septum and hippocampus. 216 40

Prolonged exposure of quiescent Swiss 3T3 cells to vasopressin prevents mitogenic stimulation on subsequent addition of bombesin. This heterologous desensitization is selective and can be mimicked by vasopressin agonists, including [Lys8]vasopressin and oxytocin but not by the V1-type-specific vasopressin receptor antagonist [Pmp1,O-Me-Tyr2,Arg8]vasopressin [where Pmp is 1-(beta-mercapto-beta,beta-cyclopenthamethylene propionic acid)]. Furthermore, vasopressin-induced loss of responsiveness to bombesin can be blocked by addition of this antagonist, indicating that heterologous desensitization is mediated through the vasopressin receptor. Desensitization requires prolonged incubation (half-maximal desensitization occurring after approximately 20 hr of pretreatment) and continuous protein synthesis. Bombesin responsiveness is restored by incubation in the absence of vasopressin. Pretreatment does not alter the number, affinity, or internalization capacity of the bombesin receptors. However, the induction of the protooncogene c-fos by bombesin is profoundly inhibited after vasopressin pretreatment. We suggest that the coupling of the activated bombesin receptor to the generation of its early signals is impaired in desensitized cells.
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PMID:Heterologous desensitization of bombesin-induced mitogenesis by prolonged exposure to vasopressin: a post-receptor signal transduction block. 254 35


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