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At least 19 recordsLinked to original sources
PubMed1976

[Milk ejection in goats and its influencing by feed].

By means of an experimental i.v. and i.m. oxytocin administration the quantitative relation between the amount of oxytocin and the quantity of ejected milk in goats was confirmed. With increasing oxytocin doses the latency period after the i.v. administration shortened, from 0.33 min. after 50 mU to 0.21 min. following 1000 mU. After the 2000 mU dose the latency period did not substantially change any more (0.18 min). The situation was nevertheless different after the i.m. oxytocin administration. No ejection followed after the 50 mU dose. Beginning with the 500 mU dose the latency period shortened, from 2.91 min. to 1.30 min. after the 2000 mU dose. With both administration manners the ejection time was prolonged up to the 1000 mU dose, then it did not substantially change. Similarly also the amount of ejected milk increased with the two administration methods up to 1000 mU, amounting to 20.6% after the i.v. and to 17.9% after i.m. administration. After 2000 mU the amount of milk ejected failed to substantially change, amounting to 19.4% with both administration manners. In experiments with manual udder stimulation with respect to feeding, the stimuli during feeding were found to influence the course of the milk ejection reflex. As compared with the pre-feeding experiments, the latency period after feeding was prolonged from 0.83 min. to 1.49 min; the amount of alveolar milk expressed in per cent of the total milk yield obtained decreased from 18.9 to 7.9%, and the ejection time shortened from 2.29 to 0.70 min. In the study the effect of various feeds on the alveolar milk ejection was also followed. Water administration did not call forth dropping off of the milk. Feeding hay called forth the ejection of 2.5% of alveolar milk occurring after an 0.25 min. latency period. Pollard provoked the ejection of 3% and the ejection time shortened from 2.29 toats (20%) can at least partially be ascribed to milk release during food intake.

Animals↗
PubMed1987

The subfornical organ and relaxin-induced inhibition of reflex milk ejection in lactating rats.

Experiments were carried out on anaesthetized, lactating rats to investigate the possible role of the subfornical organ in mediating relaxin-induced inhibition of reflex milk ejection. Milk ejection was judged by the behavioural response of the sucklings and by transient rises in intramammary pressure. Radiofrequency lesions of the subfornical organ, or control lesions in adjacent areas of the cerebrum, did not affect the pattern or the magnitude of intramammary pressure changes at reflex milk ejection. Purified porcine relaxin given by either i.v. (5 micrograms) or intracerebroventricular (50 ng) injection suppressed reflex milk ejection in intact, sham-lesioned and control-lesioned rats, but had no effect on either the pattern or magnitude of reflex milk ejection in rats with lesions of the subfornical organ. The subfornical organ, which is situated at the interface between the blood, brain and the cerebrospinal fluid appears to mediate, at least in part, the relaxin-induced inhibition of reflex milk ejection in the rat.

Animals↗
PubMed1979

Inhibitory effect of adrenaline on oxytocin release in the ewe during the milk-ejection reflex.

Milk-ejection activity was determined in the blood plasma of ewes during normal milking and during milking when adrenaline was injected intravenously before or after udder stimulation. It was found that administration of adrenaline either before or after udder washing, decreased the oxytocin concentration and milk yield but increased the yield by hand-stripping. Adrenaline also retards the average time for peak oxytocin concentration. These results and the use of a beta-receptor blocker to inhibit the effect of adrenaline at the myoepithelial cell level indicate that in ewes adrenaline can prevent the release of oxytocin from neurohypophysis.

Animals↗
PubMed1992

Aetiology of disturbed milk ejection in parturient primiparous cows.

Milk flow in nine primiparous cows with disturbed milk ejection (D) and in six corresponding control animals (C) with normal milk removal was recorded during machine milking and blood samples were taken before and during milking to determine plasma oxytocin, vasopressin, prolactin, cortisol, oestradiol-17 beta, luteinizing hormone, progesterone and beta-endorphin concentrations. Manual teat stimulation before milking lasted for 1 min. After milk flow had stopped, air was blown into the vagina for 2 min. When milk flow had stopped again, 1 i.u. oxytocin and finally 10 i.u. oxytocin were injected to remove residual milk. During and after teat stimulation, oxytocin remained basal in D, but increased in C, whereas prolactin increased in both groups. While 94% of total milk was obtained in C during this period, only 9% could be removed from D, indicating lack of alveolar milk ejection. During vaginal stimulation, oxytocin increased transiently in D and more than by teat stimulation in C. This allowed the removal of 75% of milk in D, whereas almost no more milk was available in C. After oxytocin injections, 3 and 16% of residual milk were obtained in C and D respectively. Basal oestradiol-17 beta concentration was higher in D than in C (11.6 and 2.0 ng/l respectively), whereas beta-endorphin level was lower (24.1 and 86.6 micrograms/l respectively). Basal concentration of luteinizing hormone and progesterone, and concentration of cortisol and vasopressin before and during milking were comparable in C and D. We conclude that in cows with disturbed milk ejection afferent nervous pathways to the hypothalamus were intact, because prolactin was released by teat stimulation. However, oxytocin was only released by vaginal stimulation, i.e. milk ejection was centrally inhibited during teat stimulation.

Animals↗
PubMed1992

Lesion and electrophysiological studies on the hypothalamic afferent pathway of the milk ejection reflex in the rat.

The afferent pathway of the milk ejection reflex in the hypothalamus was investigated with lesion and electrophysiological methods in anesthetized lactating rats. Destruction of the central region of the mid-hypothalamus (n = 12) blocked milk ejections induced by suckling, while that of the lateral region (n = 7) had no effect. In an electrophysiological study, extracellular recordings of neurons antidromically activated by electrical stimulation of the supraoptic nucleus were obtained from the ipsilateral hypothalamus caudal to the paraventricular nucleus (n = 84). Thirty-nine neurons were examined to see whether their firing activities changed during the milk ejection reflex. A group of 13 neurons were found to show changes in their activities prior to the reflex milk ejection; the neurons displayed a brief high-frequency burst of spikes before each milk ejection in the same manner as oxytocin neurons, and none of them antidromically responded to electrical stimulation of the neurohypophysis. The bursting neurons were recorded from the dorsomedial hypothalamic nucleus (n = 6), the region just lateral to that nucleus (n = 3) and the posterior hypothalamus (n = 4). The locations were included in a region whose destruction blocked the milk ejection reflex. These results indicate that the afferent pathway of the milk ejection reflex in the rat runs through the medial portion of the hypothalamus posterior to the paraventricular nucleus and that this region contains neurons which relay the input to the oxytocin neurons projecting in the neurohypophysis.

Afferent Pathways↗
PubMed1976

Inhibitory effect of prostaglandin F2 alpha on oxytocin release and on milk ejection in lactating rats.

The effect of prostaglandin F2 alpha (PGF2alpha) on milk ejection and on oxytocin release during suckling for one or two periods of 30 min was studied in lactating rats. Doses of PGF2 alpha (20 or 40 phi g) were injected i.p. 15 min before the suckling period. Control rats were injected with physiological saline. An inhibition of milk ejection proportional to the dose of drug administered was obtained. A normal milk ejection response was induced with a small dose of oxytocin injected immediately before nursing to mothers treated with PGF2 alpha, indicating that the blocking effect was not due to a lack of mammary gland response. Two groups of mothers were injected with 40 phi g PGF2 alpha 2 and 4 h respectively before suckling. In both groups milk ejection was partially but significantly inhibited. In rats pre-treated with sodium pentobarbitone (3-5 mg/100 g body wt) to prevent the release of oxytocin induced by suckling, PGF2 alpha (10 or 20 phi g) did not modify the inhibition of milk ejection indicating that PGF2 alpha does not have milk-ejecting activity. The administration of oxytocin to anaesthetized rats, immediately before a second suckling period, induced a normal milk-ejection response while in the rats treated with PGF2 alpha, oxytocin was less effective. The results indicate that PGF2 alpha inhibited milk ejection by a central block on oxytocin release and that the lipid is not able to mimic peripherally the milk-ejecting activity of oxytocin.

Animals↗
PubMed1990

Role of the paraventricular nucleus in controlling the frequency of milk ejection and the facilitatory effect of centrally administered oxytocin in the suckled rat.

The milk-ejection reflex was studied in anaesthetized, lactating Wistar rats in order to evaluate the contribution of the paraventricular nucleus (PVN) to the patterning of milk ejection and the facilitatory action of centrally administered oxytocin. In the first series of experiments, radiofrequency lesions were performed and centred: (1) antero-dorsal to the PVN, damaging parts of the medial septum and anterior hypothalamus; (2) in the PVN, such that much of the parvocellular division was destroyed, but parts of the magnocellular division remained intact; or (3) in the PVN, destroying both parvocellular and magnocellular divisions. Suckling tests performed before and after lesioning showed that the milk-ejection interval was significantly increased (decreased frequency) after lesioning in groups 2 and 3, but that milk-ejection amplitude was significantly decreased only in group 3. These results suggest that damage to the parvocellular division of the PVN affects milk-ejection frequency, but that damage to the magnocellular PVN only affects amplitude. Subsequent tests on rats injected into the PVN with the neurotoxin N-methyl-D,L-aspartate revealed a fall in the amplitude and frequency of milk ejection, similar to that after complete radiofrequency lesions of the PVN. In the second series of experiments, the facilitatory action of centrally administered oxytocin (1 mU, 2.2 ng) was examined in animals bearing either sham or complete PVN lesions. In both groups, intracerebroventricular injection of oxytocin was able to increase the frequency of milk ejections, although the incidence of milk ejection was lower in the pre- and post-injection period in the PVN-lesioned animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Inhibition of suckling-induced milk ejections in the lactating rat by delta 9-tetrahydrocannabinol.

The effect of delta 9-tetrahydrocannabinol (THC) on suckling-induced oxytocin release was investigated by recording intramammary pressure changes in suckled rats treated iv with THC (0.5 mg/kg BW) or vehicle. Latency to the first posttreatment milk ejection and posttreatment milk ejection intervals and pressure wave amplitudes were compared between THC- and vehicle-treated rats. Before treatment, intervals between milk ejections averaged 6.5 +/- 1.3 (+/- SE) and 7.0 +/- 0.7 min for vehicle- and THC-treated groups, respectively. Vehicle injections did not alter the frequency of milk ejections, which continued at an overall mean interval of 7.6 +/- 0.7 min after treatment. In contrast, THC treatment was followed by a transient suspension of milk ejections, with a latency of 59.3 +/- 7.4 min before the first posttreatment milk ejection was recorded (P less than 0.001). Intervals between subsequent ejections averaged 15.3 +/- 2.0 to 16.1 +/- 1.3 min and were lengthened relative to corresponding intervals in vehicle-treated animals (P less than 0.05). The amplitudes of pressure waves were not significantly affected by treatment. Oxytocin (0.5 mU) injections 10 or 30 min after THC treatment evoked abrupt increases in intramammary pressure, indicating continued responsiveness of the mammary gland to oxytocin stimulation. These data suggest that THC interferes with the release of oxytocin in response to suckling. To our knowledge, this provides the first evidence that THC inhibits posterior pituitary function.

Animals↗
PubMed1975

Isolation and some observations of the properties of a bovine neurohypophysial milk-ejecting factor.

A substance possessing milk-ejecting activity has been isolated from an acetone powder preparation of bovine posterior pituitary glands by Sephadex G-25 chromatography of the neurophysin-neurohypophysial hormone complex. While the material possessed an oxytocic activity of 2.8 IU/mg as measured on the isolated rat uterus, the milk-ejecting activity was more than three fold greater, 9.6 IU/mg. The peptide had an antidiuretic activity of 0.133 IU/mg and a pressor activity of 0.083 IU/mg. Neither the uterine-stimulating action nor the pressor activity was destroyed by incubating the peptide with 0.01 M sodium thioglycollate at 65 degrees C for 5 min. The oxytocic activity was antagonized neither by 1.4 X 10(-6) M atropine nor 3.3 X 10(-7) M phenoxybenzamine.

Amino Acids↗
PubMed1979

Milk ejection reflex linked to slow wave sleep in nursing rats.

Correlations between cerebral activity of nursing rats and the milk ejection reflex were studied in Sprague-Dawley rats with 15- to 17-day-old litters. The stretch reaction of the pups, which expresses the onset of milk ejection, was closely correlated with the slow sleep epochs of the mother. Once the litter started suckling, milk ejection only took place when the mother fell asleep and electroencephalographic features of slow wave sleep appeared. Milk ejection was never found during paradoxical sleep nor when the mother was awake. Sleep deprivation for 30 min impaired milk ejection in spite of continuous suckling of the nipples by the pups. If the mother was allowed to sleep immediately afterwards, ejection of milk occurred. A 24-h sleep-wakefulness pattern did not show differences between nursing and controls. Our results show that suckling, although necessary, is not enough to set off milk ejection. This reflex only appears when the mother falls asleep, suggesting that oxytocin release is linked to suckling and slow wave sleep.

Animals↗
PubMed1986

Regulation of the milk ejection reflex in the rat.

Extracellular recordings were made from neurones in or near the supraoptic nucleus in suckled lactating rats under urethane anaesthesia to investigate the mechanism by which the firing of oxytocin cells is synchronized during reflex milk ejection. Cells synaptically driven but not antidromically activated by neural stalk stimulation, which thus probably receive an afferent input from supraoptic neurones, were classified as 'regular' or 'bursters' on the basis of their spontaneous electrical activity. The majority (twelve out of eighteen) of synaptically excited cells (o.d.+) were bursters and the majority of inhibited (o.d.-) cells (eleven out of nineteen) were regular, but only one o.d.+ burster showed any change of activity (inhibition) before milk ejection. Putative oxytocin cells in suckled lactating rats showed a firing pattern between milk-ejection bursts which could not be distinguished from that of putative oxytocin cells in male animals. The mode interspike interval between milk ejections was 47.1 +/- 3.1 ms (mean +/- S.E. of mean) compared with 47.3 +/- 3.3 ms in male rats, and fewer than 1.4% of interspike intervals were less than 20 ms in duration. By contrast, within milk-ejection bursts 40% of interspike intervals were in the range 8-20 ms. Short trains (10 or 20) of pulses applied to the neural stalk at regular (5 min) intervals, in an attempt to simulate the initial part of the milk ejection burst, failed to trigger bursts. In only 2 of 150 tests was the interval between train and milk-ejection burst less than 10 s, and after the pulse train all but one cell showed reduced activity for 1-3 s. The trains of pulses were however not without effect: they significantly (P less than 0.01) enhanced the chance of a milk-ejection burst occurring within the next 2.5 min. Our observation that pulse trains do not trigger bursts suggests that local positive feed-back mechanisms are not responsible for orchestrating the activation of oxytocin cells during the milk-ejection reflex. Moreover, because spontaneous tiring pattern is the same in lactating and non-lactating rats, we found no evidence that the anatomical changes in the synaptic organization within the supraoptic nuclei in lactation have any influence on the firing of oxytocin cells. It is likely, however, since pulse trains alter the timing of milk ejections, that oxytocin released locally in the region of the supraoptic nucleus can influence reflex milk ejection.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1986

Blood pressure responses to milk ejection in the young rat.

When young rats receive milk ejections from their mothers they exhibit abrupt 30-50% increases in blood pressure. In our first experiment, we recorded, via carotid cannulae, blood pressure and heart rate during natural nursing bouts. Blood pressure changes coincident with behaviorally defined milk ejections were twice as large as the changes associated with other behaviors observed. In addition, the increases in blood pressure during milk ejection were significantly greater when pups were separated from their mothers for 18-20 hours prior to testing. A second experiment showed that these responses were independent of the mother's overt behavior because virtually identical results were obtained when pups received milk from anesthetized dams stimulated to release milk with oxytocin. These results are discussed with regard to possible immediate functions of the response, and long term effects of repeated cardiovascular activation in early development.

Animals↗
PubMed1986

Changing characteristics of the milk-ejection reflex during pregnancy, lactation and after weaning in the rat.

The pattern of reflex milk ejection during suckling was investigated in anaesthetized Wistar rats at various stages of pregnancy, lactation and after weaning. Milk-ejection responses were measured using intramammary pressure recordings, and the amount of oxytocin released was estimated from log dose-response lines compiled from the mammary responses to exogenous oxytocin. The number of rats showing intramammary pressure responses to oxytocin increased on Day 22 of pregnancy (the day of parturition) and decreased at 8 days after weaning. The dose-response lines from pregnant animals were shallow, but steepened and shifted to the left during lactation and after weaning. Reflex milk-ejection responses during suckling were detectable in primigravid animals, indicating that birth of the litter and previous suckling experience are unnecessary for the immediate functioning of the reflex. Reflex milk-ejection responses improved during early lactation (such that the frequency and the amount of oxytocin released at each response were maximal at Day 10 of lactation), and subsequently declined in late lactation. Although the frequency of responses in animals 2 and 4 days after weaning was similar to that in late lactating animals, the amount of oxytocin released at each response had risen again to mid-lactation values. In animals undergoing a second pregnancy and lactation the pattern of change in the milk-ejection responses was similar to that of primiparous animals.

Animals↗