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)

Influence of complete transversal section of spinal cord on secretion of hormones by hypothalamo-hypophyseal system under adaptive restoration of hyrosecretory function of kidneys was studied in chronic experiments on 28 dogs. In separate terms after the operation the level of antidiuretic hormones and oxytocin in blood plasma did not correspond to degree of organism's hydration--in contrast to intact animals. The mechanism of reciprocal secretion of hormones into the blood and CSF after the spinal section became disordered. The blood--brain barrier remained impenetrable for hormones of neurohypophysis in conditions of the spinal trauma.
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PMID:[Secretion of neurohypophyseal hormones following partial exclusion of peripheral reflex connections]. 47 30

The aim of the present study was to investigate whether amperozide, an antipsychotic drug which possesses anti-aggressive and anxiolytic-like properties, stimulates the secretion of oxytocin and if so, by which receptor mechanism. For this purpose, female or male Sprague Dawley rats were given amperozide (0.5, 2.5 and 5.0 mg/kg IP), ritanserin (5.0 mg/kg), raclopride (2.0 mg/kg) and prazosin (1.0 mg/kg) and were subsequently decapitated for collection of blood (30 and 120 min) after injection. Oxytocin levels were measured with radioimmunoassay. Amperozide 2.5 and 5 mg/kg increased plasma levels of oxytocin significantly (P < 0.05 and < 0.001). The effect appeared maximal about 30 min after injection of the drug and oxytocin levels were almost back to basal within 120 min. Similar effects were obtained in female and male rats as well as in animals that were freely fed or food deprived for 24 h. CSF levels of oxytocin were also increased. Ritanserin, a 5-HT2-receptor antagonist but not the D2 receptor antagonist raclopride or the alpha 1-adrenoceptor antagonist prazosin stimulated oxytocin release. In addition, clozapine, a neuroleptic with potent HT2-antagonistic properties, was a potent releaser of oxytocin, whereas haloperidol was without effect. A possible role for oxytocin in the behavioural effects of amperozide and clozapine remains to be explored.
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PMID:Amperozide and clozapine but not haloperidol or raclopride increase the secretion of oxytocin in rats. 136 65

It is clear that the behavioral actions of oxytocin and vasopressin in mammals are not newly acquired, but have evolutionary antecedents. Injection studies with fish, amphibians, reptiles, and birds indicate that AVT can activate certain reproductive behaviors. The strongest evidence that AVT acts centrally to control reproductive behaviors comes from research on T. granulosa. In this amphibian, injections of AVT agonists activate courtship behaviors (amplectic clasping) in males and egg-laying behaviors in females, whereas injections of AVT antagonists inhibit the behaviors. Also, in Taricha males, AVT concentrations in specific brain areas are associated with the expression of courtship behaviors. Several conclusions about steroid-peptide interactions can be drawn, based on research with this amphibian. First, gonadal steroid hormones act to maintain the behavioral actions of AVT in both males and females. In Taricha, gonadectomy abolishes and steroid implants restore AVT-induced courtship in males and egg-laying in females. Second, gonadal steroids maintain the behavioral actions of AVT, in part, by modulating AVT receptor numbers on target neurons. In Taricha males and females, gonadectomy reduces AVT receptor concentrations (but not binding affinity) in certain brain areas (amygdala pars lateralis) and not others. Third, the type of gonadal steroid determines whether AVT elicits male-like or female-like reproductive behaviors. Ovariectomized Taricha females respond to AVT injections with egg-laying behaviors when implanted with estradiol and with male-like amplectic clasping when implanted with dihydrotestosterone. Fourth, the masculinization of AVT-induced behaviors in females most likely reflects site-specific actions of androgens on AVT-synthesizing neurons. In Taricha, AVTir concentrations in the optic tectum are sexually dimorphic (higher in males than females) and reach peak levels in males during the breeding season. Fifth, AVT content in specific brain areas increase as a function of performing the behaviors. In Taricha, AVTir concentrations in DPOA, CSF, and ventral infundibulum are higher in males that exhibit courtship behaviors than in males that do not. These conclusions illustrate how steroid-peptide interactions in the control of behaviors entail multiple neuroanatomical sites and neurochemical actions.
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PMID:Evolutionary precedents for behavioral actions of oxytocin and vasopressin. 162 27

The inhibition of food intake in rats that results from various anorexigenic treatments is frequently associated with pituitary secretion of oxytocin (OT), but is not caused by circulating OT. We, therefore, evaluated the potential role of brain OT in mediating anorexia induced in rats by systemic administration of cholecystokinin (CCK), hypertonic saline (HS), or lithium chloride (LiCl), treatments that are known to stimulate pituitary OT secretion as well as to inhibit food intake. Food intake was analyzed in 22-h food-deprived rats pretreated with icv injections of either artificial cerebrospinal fluid (aCSF) or 9 nmol of an OT receptor antagonist, [d(CH2)5, Tyr(OMe)2,Orn8]vasotocin (OVT), which was the dose found to be most effective to antagonize the anorexia induced by CCK and HS. Pretreatment with the OT receptor antagonist icv significantly blunted the anorexigenic effect of each agent. After CCK (10 micrograms/kg, ip), food intake increased from 28 +/- 5% of basal intake after a CSF icv to 48 +/- 8% after OVT icv (P less than 0.01); after HS (2 ml 2 M NaCl, ip), food intake increased from 9 +/- 4% of basal intake after aCSF icv to 43 +/- 7% after OVT icv (P less than 0.01); and after LiCl (1.125 mmol/kg, ip), food intake increased from 55 +/- 4% of basal intake after a CSF icv to 80 +/- 9% after OVT icv (P less than 0.01). These data support the hypothesis that pituitary secretion of OT after anorexigenic treatments in rats is associated with coactivation of centrally projecting brain OT pathways, some of which are causally related to the induced inhibition of food intake.
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PMID:Brain oxytocin receptor antagonism blunts the effects of anorexigenic treatments in rats: evidence for central oxytocin inhibition of food intake. 164 46

The influence of naloxone on the release in limbic brain areas of both oxytocin (OXT) and vasopressin, measured by radioimmunoassay, was studied in conscious parturient rats. Three consecutive 30-min push-pull perfusions (20 microliters artificial CSF/min) were made, via previously implanted guide cannulae, within the medio-lateral septum and dorsal hippocampus of parturient animals given saline or naloxone hydrochloride (5 mg/kg body weight) after delivery of the second pup. OXT release in the hippocampus, but not in the septum, was increased during parturition, compared to day 1 post partum. During the first 30-min collection period following naloxone administration, release of OXT was significantly elevated within the septum (44% compared to saline controls, p less than 0.002), but not in the dorsal hippocampus; vasopressin release was not affected. In contrast, on day 1 post partum, naloxone, administered 5 min after starting two consecutive perfusions failed to alter OXT release in septum or hippocampus in conscious rats. Naloxone, known to increase the release of OXT also from the posterior pituitary during parturition, speeded the parturition process significantly between the birth of pups 4 and 8 during push-pull perfusion of septum or hippocampus. The data suggest that endogenous opioid inhibition is involved in the regulation of central OXT release, but not vasopressin release, during parturition. Together with previous studies on OXT release from the posterior pituitary, it seems that during parturition there is coordinated endogenous opioid action on the release of OXT both into blood and into the brain.
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PMID:Naloxone increases the release of oxytocin, but not vasopressin, within limbic brain areas of conscious parturient rats: a push-pull perfusion study. 178 42

In food-deprived male rats IP injection of cholecystokinin octapeptide (CCK-8, 5 micrograms), ingestion of food or ejaculation caused a comparable increase in plasma concentrations of CCK-8 and inhibited food intake. IV injection of 0.1 microgram CCK-8 interrupted ongoing feeding and greatly increased plasma CCK-8 levels. Osmotic minipumps delivering 0.5 micrograms CCK-8/h implanted IP reduced meal size and caused a modest increase in plasma CCK-8 levels. Injection of 5 micrograms CCK-8 IP produced an abrupt but transient increase in plasma CCK-8 concentrations whereas plasma concentrations of CCK-8 increased gradually with feeding. Injection of 5 micrograms CCK-8 IP, but not feeding, caused a marked increase in plasma oxytocin levels. The suppression of feeding, but not the increase in oxytocin, induced by IP CCK-8 was reversed by ICV injection of the CCK antagonist proglumide in a dose (100 micrograms) which failed to affect food intake if injected IP. Deprivation of food decreased and feeding increased the concentration of CCK-like immunoreactivity in the CSF. It is suggested that CCK-8 inhibits feeding in physiological doses by a specific mechanism in which peripheral as well as central neural CCK is involved.
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PMID:Relationship between the concentration of cholecystokinin-like immunoreactivity in plasma and food intake in male rats. 208 18

Oxytocin is a hypothalamic neuropeptide with both centrally and peripherally directed pathways. Data from experimental animals indicate that oxytocin impairs consolidation of aversively conditioned behaviors and is released after feeding or experimental gastric distension. The authors report that the mean CSF oxytocin level of five underweight women with restricting anorexia, but not 12 underweight bulimic anorexic women or 35 normal-weight women with bulimia nervosa, was significantly lower than the level of 11 control subjects. Restricting anorexic patients' low CSF oxytocin levels may reflect their persistently low food intake, and this behavior may exacerbate their tendency for perseverative preoccupation with adverse consequences of food intake.
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PMID:CSF oxytocin in anorexia nervosa and bulimia nervosa: clinical and pathophysiologic considerations. 235 73

Three putative processing enzymes, each with defined action in a prohormone system, a 'pro-ocytocin-neurophysin convertase' from bovine neurohypophysis secretory granules, a 'Leu-enkephalin Arg6 generating enzyme' from human CSF and the endoprotease from the 'S-28 convertase' complex of rat brain cortex, were tested for their ability to hydrolyze peptides deriving from pro-ocytocin, pro-enkephalin B and pro-somatostatin, respectively at pairs of basic amino acids. The observations suggest that structural parameters specified by the peptide region around the dibasic moieties govern recognition by the enzyme and define which peptide bond is hydrolyzed.
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PMID:Role of peptide substrate structure in the selective processing of peptide prohormones at basic amino acid pairs by endoproteases. 289 32

The most examined tumor markers in lung cancer patients are CEA, hormonal peptides, and some neurogenic enzymes in small cell carcinoma. Calcitonin, ACTH, ADH, CEA, neurophysin, oxytocin, beta-endorphin, neuron-specific enolase, and CK BB are elevated in serum specimens in 25-75% of cases of small cell carcinoma. The level of these markers is related to the stage of the disease in groups of patients; elevated pretreatment levels decrease with tumor regression. Marker levels are not valid in defining the tumor load and the presence of disease in the individual patient. It has not yet been documented that the markers can be used for clinical decisions on antineoplastic therapy. A recent development is the finding that measurement of CSF and plasma concentrations of ADH, calcitonin, CK BB, bombesin, and neuron-specific enolase may contribute in the diagnosis of CNS metastases including meningeal carcinomatosis.
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PMID:Tumor markers in patients with lung cancer. 300 40

CSF vasopressin levels were significantly elevated in eight patients with motor neuron disease (2.5 +/- 0.4 pmol/l) compared with controls (0.7 +/- 0.1 pmol/l). CSF oxytocin and plasma vasopressin concentrations were similar in the two groups. This finding may be a primary part of the disease process or an epiphenomenon related to increased autonomic and descending pathway activity secondary to abnormal function and/or loss of anterior horn cells.
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PMID:Elevated cerebrospinal fluid vasopressin in motor neuron disease. 361 58


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