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

(1) Haloperidol, a dopaminergic antagonist was injected i.p. or into the 3rd ventricle (i.c.v.) of lactating rats to determine whether or not a dopaminergic component was involved in the reflex release of oxytocin (OT) induced by (a) vaginal dilatation (Ferguson reflex), (b) vagal stimulation (vago-pituitary reflex), (c) suckling (milk-ejection reflex). Moreover, we examined the effect of a dopaminergic agonist, apomorphine, on the milk-ejection (ME) reflex. (2) I.c.v. injection of 20 microgram haloperidol inhibited the vaginal and vagal reflexes. The inhibition of the ME reflex produced by 2, 5 or 8 mg/kg i.p. or by 20 and 40 microgram i.c.v. haloperidol was dose-dependent. Apomorphine (10 mg/kg i.p.) had no effect. (3) The results suggest that a dopaminergic component must be involved in OT release whatever the peripheral stimulus.
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PMID:Effects of dopaminergic antagonist and agonist on oxytocin release induced by various stimuli. 43 76

The isolated hypothalamo-neurohypophysial system (HNS) of male rats was incubated with putative neurotransmitters in vitro to determine their significance in regulating oxytocin release. Dopamine was found to inhibit the spontaneous release of oxytocin from the HNS in a dose-related manner. The maximum inhibition produced by dopamine (10(-9) M) was significantly different from control values and was blocked by haloperidol (5 x 10(-5) M). Apomorphine (10(-9) M) mimicked the effect of dopamine on this system. The type of receptor involved in the inhibitory effect on oxytocin release is unclear, although a dopaminergic mechanism in vivo. When levodopa plus carbidopa were injected into male rats, the gland content of oxytocin in these animals was significantly increased over control values. When a similar dosage regimen was employed with pregnant rats beginning on day 16 of gestation, levodopa plus carbidopa delayed the average delivery time 12 hr. The results of these studies are also consistent with a dopaminergic mechanism for the regulation of oxytocin release.
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PMID:Investigation of a dopaminergic mechanism for regulating oxytocin release. 71 42

1. The rat hypothalamus (containing the supra-optic nuclei, paraventricular nuclei, median eminence and proximal pituitary stalk) has been incubated in vitro and shown to be capable of releasing the neurohypophysial hormones, oxytocin and arginine vasopressin, at a steady basal rate about one twentieth that of the rat neural lobe superfused in vitro. 2. The hypothalamus and neural lobe in vitro released both hormones in a similar arginine vasopressin/oxytocin ratio of about 1-2:1. However, when release was expressed relative to tissue hormone content, the hypothalamus was shown to release about three times as much arginine vasopressin and six times as much oxytocin as the neural lobe. 3. Dopamine in a concentration range of 10(-3)-10(-9)M caused graded increases in hormone release from the hypothalamus in vitro to a maximum fivefold increase over preceding basal levels. The demonstration that apomorphine also stimulated hormone release whereas noradrenaline was relatively ineffective suggested that a specific dopamine receptor was involved. A separate cholinergic component in the release process was indicated by the finding that acetylcholine stimulated release to a maximum fivefold increase in concentrations of 10(-3)-10(-9)M. 4. The fact that the isolated hypothalamus can be stimulated by dopamine and acetylcholine to release increased amount of oxytocin and arginine vasopressin raises the question of the origin and fate of the hormones released in this way. The possibility that they could be released into the hypophysial portal circulation from median eminence to affect the anterior lobe of the pituitary is discussed. 5. In similar doses, both dopamine and noradrenaline injected into the lateral cerebral ventricles of the brain of the anaesthetized, hydrated, lactating rat caused the release of arginine vasopressin and oxytocin. Apomorphine release both hormones but at a higher dose level and to less effect than the catecholamines. 6. The hormone release induced in vivo by dopamine could be prevented by the prior administration of haloperidol or phentolamine and these antagonists were equally effective in blocking the hormone release due to noradrenaline. The involvement of a specific dopamine receptor was more clearly implicated by the use of pimozide which completely inhibited the hormone release due to dopamine and apomorphine but not that due to noradrenaline. 7. It is suggested that the release of neurohypophysial hormones can be stimulated via a dopaminergic nervous pathway in addition to a cholinergic one. The possibility that the osmoreceptor mechanism for the release of antidiuretic hormone from the neural lobe of the pituitary may involve such a dopaminergic pathway is discussed.
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PMID:The effect of dopamine on neurohypophysial hormone release in vivo and from the rat neural lobe and hypothalamus in vitro. 98 83

Apomorphine challenge tests (0.5 mg SC) were performed in 14 normal male volunteers and in 9 male schizophrenic inpatients, drug-free for at least 2 wk. In the normal volunteers, apomorphine induced an increase of serum growth hormone (GH) (maximum at 40 min), of vasopressin-neurophysin (hNpI) (maximum at 20 min), and oxytocin-neurophysin (hNpII) (maximum at 20 min). The release of neurophysins was independent of digestive side effects. In the schizophrenics, the GH level and release pattern were similar to those in the controls. The basal level of hNpI was reduced (t0: 0.42 +/- 0.1 ng/ml in the schizophrenics and 0.66 +/- 0.05 ng/ml in the controls, p < 0.02). In contrast, the basal level of hNpII was increased (3.34 +/- 0.04 ng/ml in the schizophrenics to 0.92 +/- 0.21 ng/ml in the controls, p = 0.001). The response to apomorphine was blunted, with no significant release of hNpI or of hNpII. Although the hNpII data are consistent with an increased dopaminergic tone, the psychopathological meaning of the increased basal oxytocinergic and decreased vasopressinergic functions remains to be defined.
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PMID:Apomorphine stimulation of vasopressin- and oxytocin-neurophysins. Evidence for increased oxytocinergic and decreased vasopressinergic function in schizophrenics. 128 81

Administration of the dopamine receptor agonist apomorphine causes a dose-dependent increase in plasma oxytocin concentrations and dose-specific behavioral changes in rodents. To investigate whether dopamine receptor agonists will elicit similar neuroendocrine and behavioral effects in primates, we administered graded doses of apomorphine and the respective dopamine D1 and D2 receptor agonists, CY 208-243 and LY 163502, to monkeys and monitored plasma concentrations of oxytocin and behavior. Five female rhesus, two male rhesus, and two male cynomolgus monkeys had chronic indwelling venous catheters implanted and were maintained on standard jacket/tether/swivel systems to allow remote blood sample collection. During experiments, blood samples were collected 10 and 5 min before drug injection and at 2- to 120-min intervals after each injection. Apomorphine (50-400 micrograms/kg) and LY 163502 (10-100 micrograms/kg) elicited dose-dependent stimulations of oxytocin secretion. CY 208-243 (100-400 micrograms/kg) did not significantly affect oxytocin secretion. Low doses of apomorphine (50-100 micrograms/kg) and LY 163502 (10-25 micrograms/kg) elicited yawning, and high doses of apomorphine (200-400 micrograms/kg) and LY 163502 (50-100 micrograms/kg) elicited stereotypic behaviors. No behavioral effects of CY 208-243 (100-400 micrograms/kg) were observed. The magnitude of the oxytocin secretory responses varied among animals, but was similar in male and female monkeys. In summary, apomorphine and LY 163502 both elicited dose-related stimulation of oxytocin secretion coupled with dose-specific behavioral changes in male and female monkeys, while no effects of CY 208-243 on these parameters were observed. We conclude that dopamine receptor agonists, and in particular D2 agonists, may be useful tools for studies exploring the physiological and behavioral actions of oxytocin in primates.
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PMID:Dopaminergic stimulation of oxytocin concentrations in the plasma of male and female monkeys by apomorphine and a D2 receptor agonist. 135 89

The effect of the dopamine (DA) agonist, apomorphine, on oxytocin concentrations in the hypothalamus, hippocampus, septum and plasma was studied in male rats. Apomorphine dose dependently increased the concentration of oxytocin in the plasma and hippocampus, the minimal effective dose being 80 micrograms/kg s.c., which induced a 65% increase in plasma and a 45% increase in the hippocampus. The maximal effect (210 and 125% above controls) was induced with 240 micrograms/kg s.c. In contrast, there was a significant decrease (32%) in the oxytocin concentration in the hypothalamus, but only after the highest doses of apomorphine, while no change was found in the septum. The apomorphine effect in the hippocampus and hypothalamus was prevented by the mixed DA D-1/D-2 receptor blocker, haloperidol (0.3 mg/kg i.p.), and by the DA D-2 receptor blocker, (-)-sulpiride (20 mg/kg i.p.), but not by the DA D-1 receptor blocker, SCH 23390 (0.2 mg/kg s.c.). Similar effects were found in plasma, although SCH 23390 inhibited the apomorphine effect by 45%. Our results suggest that apomorphine stimulates oxytocinergic transmission in male rats and provide biochemical support for the hypothesis that a DA-oxytocin link exists in the central nervous system.
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PMID:Effect of apomorphine on oxytocin concentrations in different brain areas and plasma of male rats. 220 5

The effect of systemic administration of the dopamine agonist apomorphine on plasma oxytocin concentration was studied in male rats by a specific radioimmunoassay. Apomorphine given subcutaneously in doses ranging from 80 to 480 micrograms/kg increased oxytocin levels in a dose-dependent manner. The minimal effective dose was found to be 80 micrograms/kg, which induced a 66% increase above basal values, while the maximal effect (210%) was seen with a dose of 240 micrograms/kg. The apomorphine effect was prevented by pretreatment with the DA D2-receptor blockers haloperidol (0.2 mg/kg i.p.) or (-) sulpiride (10 mg/kg i.p.) and, but only partially, with the DA D1-receptor blocker SCH 23390 (0.2 mg/kg s.c.). The present results suggest that hypothalamic dopamine has a facilitatory role on the release of oxytocin in male rats.
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PMID:Apomorphine increases plasma oxytocin concentration in male rats. 265 6

The effect of the intracerebroventricular (ICV) injection of the oxytocin antagonist d(CH2)5Tyr(Me)-Orn8-vasotocin on the stimulation of copulatory behavior induced by the dopamine (DA) agonist apomorphine was studied in male rats. Apomorphine (80 micrograms/kg SC) given 5 min before mating tests decreased intromission frequency and ejaculation latency in experienced male rats. Such effects were abolished and reversed by pretreatment with 50 and 1000 ng of the oxytocin antagonist given ICV 5 min before apomorphine. The peptide per se markedly increased intromission and ejaculation latency and abolished ejaculation in control rats. The results suggest that brain oxytocin is implicated in the expression of sexual behavior, and apomorphine might improve male copulatory behavior by releasing oxytocin in brain.
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PMID:Apomorphine stimulation of male copulatory behavior is prevented by the oxytocin antagonist d(CH2)5 Tyr(Me)-Orn8-vasotocin in rats. 278 Jul 93

Apomorphine, a centrally-acting emetic, was administered subcutaneously (50 micrograms/kg) to nine normal subjects (four male, five female; aged 22-36 years) and four patients with idiopathic diabetes insipidus (DI) (one male, three female; aged 24-49 years). In the normal subjects this stimulus caused nausea (and vomiting in seven of nine) with a latency of 9.5 +/- 0.9 min which was followed by a large increase in plasma arginine vasopressin (AVP) concentration (from 0.9 +/- 0.2 pmol/l to 249 +/- 104 pmol/l at 15 min after the onset of symptoms; mean +/- SEM, P less than 0.01). There was a small but significant increase in plasma oxytocin (OXT) concentration (from 1.6 +/- 0.4 pmol/l to 6.2 +/- 3.4 pmol/l; P less than 0.05). Mean arterial pressure (MAP) fell slightly (from 87 +/- 1.9 mm Hg to 71 +/- 4.4 mm Hg; P less than 0.05) 15 min after the onset of nausea; there was no change in blood haematocrit or plasma osmolality and sodium concentration. In the DI patients apomorphine produced nausea (with vomiting in three of four) with a latency of 10.0 +/- 1.4 min but failed to cause an increase in either plasma AVP or OXT. In the DI patients the fall in MAP did not reach statistical significance (83 +/- 4 mm Hg to 71 +/- 11 mm Hg); there was also no change in haematocrit, osmolality or sodium concentration. Ipecacuanha, an emetic with both peripheral and central actions, was administered orally to seven normal subjects (three male, four female; aged 22-36 years) six of whom also underwent apomorphine tests.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Responses of plasma oxytocin and arginine vasopressin to nausea induced by apomorphine and ipecacuanha. 290 23

1-(3-Chlorophenyl)piperazine (m-CPP) (0.1-4 mg/kg s.c.) and N-(3-trifluoromethylphenyl)-piperazine (TFMPP) (0.5-4 mg/kg s.c.), 5-HT1C receptor agonists, but not 8-hydroxy-dipropylamino-tetralin (8-OH-DPAT) (0.1 and 0.2 mg/kg s.c.), a 5-HT1A receptor agonist, induced penile erection and yawning with a U-inverted dose-response curve in male rats. The maximal effect was found with 0.5 mg/kg s.c. of m-CPP and with 1 mg/kg s.c. of TFMPP. The m-CPP (0.5 mg/kg s.c.) and TFMPP (1 mg/kg s.c.) responses were prevented by mianserin (0.2 mg/kg s.c.) and by ritanserin (1 mg/kg s.c.) given 15 min before m-CPP and TFMPP. In contrast, m-CPP- or TFMPP-induced penile erection and yawning were not antagonized by haloperidol (0.1 mg/kg s.c.) or by [d(CH2)5Tyr(Me)2,Orn8]vasotocin (5 micrograms i.c.v.). Apomorphine- and oxytocin-induced penile erection, but not yawning, was also antagonized by mianserin and less effectively by ritanserin. The results suggest that 5-HT1C receptor agonist-induced penile erection and yawning are not mediated by increased dopaminergic and/or oxytocinergic transmission, and raise the possibility that a neuronal dopamine-oxytocin-5-HT link is involved in the control of penile erection and not necessarily of yawning in male rats.
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PMID:Penile erection and yawning induced by 5-HT1C receptor agonists in male rats: relationship with dopaminergic and oxytocinergic transmission. 800 37


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