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)

Lesions of the median raphe (MR) nucleus were placed in cycling female rats and their ability to lactate was evaluated following subsequent pregnancies. Pups from MR-lesioned (MRL) animals grew more slowly and had greatly impaired survival rates compared to pups from sham-lesioned animals. Chronic treatment of MRL mothers with oxytocin (Oxy; 1 IU, s.c., once or twice/day) did not increase the growth rates of their litters. Acute responses to exogenous Oxy (1 IU, i.p.) in MRL mothers, measured by the weight gain of litters during 1/2-h suckling intervals before and after injection, were marginally significant. Milk yield during the total hour suckling period (stomach contents of pups) was clearly less in the MRL animals (p less than 0.01). Treatment with either prolactin (Prl; 250 microgram, twice/day), Prl + GTC (4 mg/kg gorwth hormore, 30 microgram/kg thyroxine, 0.5 mg/rat cortisol, once/day), or 5-HTP (75 mg 5-hydroxytryptophan/kg, twice/day) did not improve the growth rates of litters from MRL animals. However, when milk yield (stomach contents after 1 h) following a 14-h non-suckling interval was measured, lactogenic hormones (Prl or Prl + GTC) restored milk yield in MRL animals to control levels. This response was clearly not dependent upon exogenous Oxy. These results suggest that deficits in the release of lactogenic hormones are involved in the impairments in lactation following lesions of the MR nucleus.
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PMID:Impairments in lactation in the rat following destruction of the median raphe nucleus. 69 8

Serotonergic control over the reflex oxytocin (OT) release was investigated in anesthetized rats and in conscious rats. The effects of drugs were tested in the first case, on the electrical activity of oxytocinergic cells during sucklings and in the second case, on the litter weight gain after 30 min suckling (indirect index of OT release). In rats anesthetized with urethane (1.2 g/kg), intraventricular injection of 1 microgram serotonin interrupted the regular pattern of the neurosecretory bursts and milk ejections for about 15-20 min (inhibitory effect of the 'all-or-none' type). 10 micrograms cyproheptadine or R47465 (serotonergic antagonists) slightly but significantly decreased the mean delay between two neurosecretory bursts without modifying their amplitude and in half the cases, disturbed their periodicity with occasional appearance of very close dual neurosecretory bursts. Pretreatment with rho-chlorophenylalanine (PCPA) (250 mg/kg i.p.) did not prevent or affect the regular milk ejection pattern. The inhibitory effect of 5-HT was lengthened by fluoxetine, a 5-HT reuptake inhibitor (1 microliter of 10(-4) M solution into the 3rd ventricle) and prevented by 5 micrograms R47465. In conscious rats, all the above drugs had an opposite effect. 5-HT and 5-HTP (5-HT precursor) did not affect the milk ejection reflex, whereas serotonergic antagonists and PCPA had an inhibitory effect. Injecting 5-HT into the PCPA-treated mothers restored their ability to release OT in response to suckling. Hypotheses for these opposite effects are discussed.
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PMID:Serotonergic control of oxytocin release during suckling in the rat: opposite effects in conscious and anesthetized rats. 622 33

Chronic hyponatremia is known to cause inhibition of pituitary vasopressin (AVP) and oxytocin (OT) secretion in response to most physiological stimuli, as well as a marked inhibition of synthesis of these peptides. Because many studies have implicated neurohypophyseal peptides in the regulation of pituitary prolactin (PRL) secretion, we investigated the effects of chronic hyponatremia on basal and stimulus-induced PRL secretion in rats. Hyponatremia was induced by subcutaneous infusion of 1-deamino-[8-D-arginine]-vasopressin (dDAVP) (5 ng/h) to rats fed a nutritionally balanced liquid diet, and plasma [Na+] was maintained < or = 115 mmol/l for 10-12 days. After this period, hyponatremic rats and normonatremic controls fed the same diet without dDAVP were subjected to one of the following stimuli known to stimulate PRL release in rats: 3 min exposure to ether, hemorrhage (20 ml/kg), intravenous injection of 5-hydroxytryptophane (5-HTP, 10 mg/kg), or intravenous injection of estradiol (5 micrograms/kg). A baseline blood sample was collected before each stimulus, and 3-6 additional blood samples were collected at selected intervals after the stimulus. Baseline levels of plasma PRL were not different between normonatremic and hyponatremic rats. However, PRL responses induced by either or estradiol, but not those induced by hemorrhage or 5-HTP, were very significantly blunted in the chronically hyponatremic rats. Plasma AVP and OT responses were measured as an index of magnocellular secretion, but did not correlate with the PRL responses for any of the stimuli tested.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Osmotic inhibition of prolactin secretion in rats. 792 May 95