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PubMed1988

Activation of the adrenal cortex or the peripheral sympatho-adrenomedullary system does not necessarily influence milk ejection in the rat.

Following a 5-h isolation period, primiparous rats have the same milk supply on days 8/9 and 13/14 post partum, yet in response to suckling they release a greater amount of milk at the latter time. Inasmuch as stress is known to inhibit lactation and handling of the pups is stressful to the dams, the question arose as to whether separation from pups before nursing constitutes a greater stress for the dam at the earlier stage of lactation. This possibility was explored in the present study: As an index of stress, changes in plasma corticosterone were measured from chronically cannulated dams. In addition, the role of adrenal hormones and the peripheral sympathetic nervous system in the regulation of milk ejection under these experimental conditions was assessed following bilateral adrenalectomy and treatment with pentolinium, a ganglionic blocker which does not cross the blood-brain barrier. Corticosterone pellets were implanted subcutaneously following adrenalectomy in order to maintain proper lactation. From the results obtained, lactators demonstrated a greater increase in plasma adrenocorticosteroid levels in response to nursing on day 8/9 than on day 13/14 post partum, but milk yield was significantly less at the earlier than at the later stage of lactation. Adrenalectomy in conjunction with corticosterone replacement pellets did not alter milk supply or milk release. The subsequent treatment with pentolinium did not affect milk ejection. Pups still ingested less milk on day 9 than on day 13/14. It is suggested here that the isolation/suckling condition imposed on lactators may be more stressful earlier in lactation. Inasmuch as removal of the adrenal hormones along with ganglionic blockade did not modify the amount of milk ingested by the pups, it is concluded that the smaller milk release observed on day 9 post partum does not result from a direct suppression by the adrenal hormones or by the peripheral sympathetic nervous system on milk ejection.

Adrenal Cortex↗
PubMed1995

Mortyn Jones Memorial Lecture. Limbic regions mediating central actions of oxytocin on the milk-ejection reflex in the rat.

Central oxytocin administration has a profound facilitatory effect on the patterning of the milk-ejection reflex in the lactating rat. Lesion and microinjection studies indicate that this action is, in part, mediated via a population of limbic neurones in the bed nuclei of the stria terminalis and ventrolateral septum, which have been shown to possess oxytocin receptors and to be activated by selective oxytocin-receptor agonists in vitro. In vivo electrophysiological recordings reveal that some of these neurones display cyclical activity which is highly correlated to each milk ejection, and are rapidly activated following i.c.v. administration of oxytocin, coincident with the facilitation of milk ejection activity. A hypothetical model is proposed in which this population of limbic neurones serves to gate the activity of a pacemaker which, in turn, coordinates the bursting of hypothalamic magnocellular neurones. The oxytocin innervation of these neurones and their expression of oxytocin receptors increases in the postpartum period, and the resultant enhanced sensitivity leads to a greater facilitatory response during lactation. Inhibitory opioid and noradrenergic inputs which converge on these oxytocin-sensitive neurones may function to switch off the facilitatory circuit during periods of stress. Thus, this population of limbic neurones participates in the regulation of neuroendocrine activity during lactation by providing an appropriate degree of feedback to alter the patterning of the milk-ejection reflex.

Animals↗
PubMed1981

Excitatory effects of intraventricular injections of oxytocin on the milk ejection reflex in the rat.

The effects of oxytocin, administered into the 3rd cerebral ventricle, on the milk ejection reflex, were studied in urethane-anaesthetized lactating rats. Intramammary pressure, electrical activity of oxytocinergic neurones and EEG were recorded simultaneously. Intraventricular injection of oxytocin (6, 60 and 600 microU) significantly increased both milk ejection frequency and the number of spikes in the oxytocinergic neurones characteristic bursts. The amount of hormone released for each milk ejection was higher after intraventricular oxytocin injection than before. The strongly excitatory effect of intraventricular oxytocin injection on the milk ejection reflex was not reproduced with arginine-vasopressin.

Animals↗
PubMed1989

Release of oxytocin within the supraoptic nucleus during the milk ejection reflex in rats.

To investigate the hypothesis that oxytocin may be released within the magnocellular nuclei in vivo, push-pull cannula perfusions were performed in anaesthetized lactating rats in one supraoptic nucleus of the hypothalamus while recording the intramammary pressure and/or the electrical activity of oxytocin cells in the contralateral supraoptic nucleus. Oxytocin content was measured in samples collected over 15 min, under various conditions: 1) with no stimulation; 2) during suckling and suckling-induced reflex milk ejections; 3) during electrical stimulation of the neuro-hypophysis by trains of pulses that mimicked oxytocin cell bursts; 4) under osmotic stimulation by i.p. injection of 2 ml of 1.5 M NaCl to evoke a tonic and sustained oxytocin release from the neurohypophysis. Oxytocin release within the supraoptic nucleus increased significantly during the milk ejection reflex and, to a lesser extent, during burst-like electrical stimulation of the neurohypophysis. In suckled rats, the increase started before the first reflex milk ejection occurred. There was no apparent correlation between the amount of oxytocin in the perfusates and the number of milk ejections and oxytocin cell bursts occurring during each perfusion period. The amount of oxytocin in the perfusates further increased-during facilitation of the milk ejection reflex by intraventricular injections of oxytocin or its analogue, isotocin. When suckling failed to evoke the milk ejection reflex, there was no change in intra-supraoptic oxytocin release. There was also no change after osmotic stimulation. When the push-pull cannula was positioned outside the supraoptic nucleus, there was no increase in the amount of oxytocin during the three types of stimulation tested. These results provide evidence for an endogenous release of oxytocin within the magnocellular nuclei in lactating rats. It is suggested that the increase in such a release induced by suckling is likely to be a prerequisite for the onset and the maintenance of the characteristic intermittent bursting electrical activity of oxytocin cells leading to milk ejections.

Animals↗
PubMed1982

Electrical activity of septal neurones during suckling and the milk ejection reflex in the lactating rat.

Extracellular recordings from neurones in the lateral septum were performed in urethane anaesthetised lactating rats to study the eventual role of the septum in the control of suckling-induced oxytocin release. The connections of these neurones with the supraoptic nucleus, which contains cells secreting oxytocin, were assessed electrophysiologically by single pulse stimulation of the ipsilateral supraoptic nucleus. The neurones were thus classified into four categories: antidromically activated, orthodromically activated or inhibited, and unresponsive neurones. One hundred septal neurones were recorded in animals not exposed to suckling. A second group of 40 cells were analysed during suckling and one or more reflex milk ejections. The mean firing rates of each category of septal neurone did not differ significantly during suckling from the values observed in the absence of suckling. During suckling, almost all the recorded septal cells showed no significant alteration in their level of firing in relation to milk ejections. Two neurones presented an activation in the period between two milk ejections that seemed related to arousal. One neurone was clearly inhibited at the time of milk ejection. Our observations suggest that the septum does not represent an essential component of the pathways necessary for the milk ejection reflex induced by suckling, although it could exert an inhibitory action modulating either the intervals between two successive milk ejections, or the amount of oxytocin released.

Animals↗
PubMed1982

[Efficacy of PGF2 alpha on milk ejection during the sexual cycle of the cow].

After 30 days of lactation, 15 non-pregnant French Friesian cows were divided into groups A and B, balanced by the milk yield and lactation number of the cows. The 7 cows of group A were given a series of intrajugular prostaglandin F2 alpha (Upjohn Dinolytic) injections every morning, administered in increasing logarithmic doses (1, 4, 16, 64, 256, 1 024 micrograms). The aim of the experiment was to determine the minimal dose that would induce an increase in intramammary pressure (IMP) during the sexual cycle and milk let-down through a cannula in the teat cup. The 8 cows of group B were given a single injection of 256 micrograms of PGF2 alpha every morning to determine the changes during the sexual cycle in the response parameters of IMP (latency and amplitude) or of milk let-down (latency and collected volume) through a cannula. The following results were obtained: 1. The minimal dose of prostaglandin inducing milk let-down varied during the cycle; it was lower (1 to 16 micrograms) during the luteal phase (D4 to D12) than during the perioestral phase (256 to greater than 1 024 micrograms from D - 2 to D + 3) (figs. 2, 3). 2. During daily administration of the same dose (256 micrograms) of PGF2 alpha no response was obtained during the perioestral phase, while during the luteal phase; - maximal IMP deflection reached 12 to 14 mmHg (figs. 5, 6); - the volume of milk ejected was on an average higher than 3 liters per quarter (figs. 5, 6); - the latency time between injection and let down response was about 1.8 times shorter between D10 and D12 than between D4 and D5 (fig. 7). 3. The cyclic changes in the milk ejection parameters caused by PGF2 alpha were closely related to the plasma progesterone level (figs. 2, 3, 5, 6). The coefficients of correlation between the progesterone level and the - threshold dose: r = - 0.809** (group A), - volume of ejected milk: r = + 0.872*** (group B), - deflection amplitude: r = + 0.805*** (group B) were always significantly higher than the threshold of 0.001. Various hypotheses concerning the endocrine control of cyclic variations in milk let-down under the effect of PGF2 alpha are discussed.

Animals↗
PubMed1985

Somatosensory systems and the milk-ejection reflex in the rat. I. Lesions of the mesencephalic lateral tegmentum disrupt the reflex and damage mesencephalic somatosensory connections.

Bilateral electrolytic lesions and unilateral tracer injections were performed in lactating rats in order to study the participation of the mesencephalic lateral tegmentum in the milk-ejection reflex. The release of oxytocin was detected as a rise in intramammary pressure during each milk ejection. In animals with lesions, the lateral part of the deep grey layers of the superior colliculus, the intercollicular area and the rostromedial portion of the external nucleus of the inferior colliculus were destroyed. The mesencephalic lateral tegmentum of animals in which the milk-ejection reflex was blocked sustained a larger damage than in rats where the frequency of the milk-ejection response was only slowed down. Solutions of True Blue, horseradish peroxidase or horseradish peroxidase coupled to wheat germ agglutinin were injected in the mesencephalic lateral tegmentum of rats with and without lesions. Retrogradely labelled cells were found in several nuclei of the somatosensory pathways: the principal sensory and spinal parts of the trigeminal complex, the cuneate and gracile nuclei, the lateral cervical nucleus and the nucleus proprius of the spinal cord. Labelled cells were also found in the ventral nucleus of the lateral lemniscus, the ventral parabrachial nucleus, the gigantocellular reticular nucleus, the lateral nucleus of the substantia nigra, the prerubral nucleus of the thalamus, the hypothalamic ventromedial nucleus, the zona incerta and in the anterior and lateral hypothalamic areas. Labelled fibres and "terminal-like" labelling were found in the anterior pretectal area, in the thalamic parafascicular nucleus, in the posterior nucleus and the ventroposterior complex, in the zona incerta and in the fields of Forel, but none were observed in the supraoptic or paraventricular nuclei. Injections made in the area of the lateral cervical nucleus and in the cuneate and gracile nuclei labelled fibres and "terminal-like" fields in the external nucleus of the inferior colliculus, the intercollicular area, the deep grey layers of the superior colliculus and in the mesencephalic lateral tegmentum. After injections in the posterior nucleus and ventroposterior complex of the thalamus, retrogradely labelled cells were found in the lateral tegmentum, the intercollicular area and the external nucleus of the inferior colliculus. These results indicate that bilateral lesioning of the mesencephalic lateral tegmentum, which disrupts the milk-ejection response, could damage somatosensory projections originating from the dorsal horn of the spinal cord, the lateral cervical nucleus, the dorsal column nuclei and the sensory and spinal trigeminal nuclei.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2004

Changes of physicochemical indicators during mastitis and the effects of milk ejection on their sensitivity.

We examined the relationship between physicochemical indicators and somatic cells in the milk of dairy cows during experimentally induced mastitis and their significance as indicators for use in controlling udder health. We were concerned particularly with the effect of alveolar milk ejection on the sensitivity of these indicators. In Expt 1, Escherichia coli lipopolysaccharide (Esch. coli LPS) was injected into the left rear quarter to induce an inflammatory reaction in one quarter in each of six cows. The contralateral control quarter was injected with a solution of NaCl (9 g/l). Nine milk samples were taken from both quarters until 60 h after injection. In Expt 2, repeated milk samples were taken every 20 s from one quarter during a 120-s teat stimulation in 20 cows with different somatic cell counts (SCC). Quarters were clustered for low (<5.0 log cells/ml), mid (5.0-5.7 log cells/ml) and high (>5.7 log cells/ml) SCC of the sample taken at t=0 s. Samples were analysed for SCC, electrical conductivity (EC) and Na+ and Cl- concentrations. During the experimental inflammation SCC, EC, Na+ and Cl- peaked at 12 h from LPS administration and values in treated quarters (T) at this time were elevated to 7900, 157, 501 and 169% of the values in untreated quarters, respectively. In Expt 2, SCC, EC, Na+ and Cl- in high SCC quarters were 2520, 121, 283 and 141% of low SCC quarters at the start of stimulation (t=0 s), respectively. Highly significant (P<0.001) differences in EC, Na+ and Cl- between high and low SCC quarters disappeared owing to the onset of alveolar milk ejection 100 s after the first contact with the teat. In conclusion, SCC in cows' milk provided the strongest amplitude in the case of an intramammary inflammation. EC, Na+ or Cl- were useful tools only if the measurements were performed in cisternal milk before the start of alveolar milk ejection.

Animals↗
PubMed2004

Effects of oxytocin administration on oxytocin release and milk ejection.

In experiment I, the effect of i.m. oxytocin (OT) injection (50 IU) on OT blood pattern was tested. Blood samples from 6 cows were collected for 2 h after OT injection either with or without milking. To test the effect of i.m. OT injection (50 IU) on milk ejection efficiency, intramammary pressure (IMP) was measured in 13 cows (experiment II). Milk ejection was induced by manual teat stimulation. After IMP increased and reached a plateau, OT was injected. In experiment III, the effect of chronic OT treatment on mammary gland sensitivity and endogenous OT release was tested. For 19 d, cows were i.m. injected at each milking with 50 IU OT (n = 13) or 5 mL of NaCl 0.9% (n = 14) 1 min before the start of udder preparation. To test mammary gland sensitivity, IMP recording was performed after a long (11 h, 7 OT cows, and 7 NaCl cows) and a short (3 h, 6 OT cows, and 7 NaCl cows) milking interval at d -1 and d 18. To test the effect of withdrawal of chronic i.m. treatment on OT release, blood sample collection was performed during evening milking at d 0 and d 19. Intramuscular oxytocin injection (experiment I) caused elevated OT blood levels observed at least for 2 h and showed an even more pronounced effect when milking was also performed. Intramuscular OT injection after teat stimulation (experiment II) caused additional milk ejection but only in 6 out of 13 cows. Withdrawal of chronic OT treatment (experiment III) did not reduce OT release during milking. However, ejection time was prolonged during OT infusion after a long milking interval. Ejection pressure tended to be lower after a short milking interval. It seems that the reduction of spontaneous milk removal after chronic OT treatment was due to reduced contractibility of myoepithelial cells in the mammary gland at a physiological range of OT concentrations.

Animals↗
PubMed1975

Pattern of sucking in the infant rat during spontaneous milk ejection.

Two methods are described for measuring the sucking of rat pups on the nipples of the mother. The first uses pressure recording of the cannulated teatduct; the second uses direct observation of sucking behavior. Using these methods, the sucking behavior of the pups during sequences of milk ejections was investigated. Pressure recordings of the sucking of individual pups on the nipple showed that between milk ejections the pups sucked intermittently in bursts. During milk ejection itself there was a longer period of vigorous and continuous sucking. Behavioral observations on the level of sucking in whole litters of pups showed that the background bursts of sucking from the litter as a whole were randomly distributed in relation to the inferred time of oxytocin release. These results indicate that once the pups are sucking on the nipples, variations in the sucking behavior of the litter have no role in the timing of milk ejections in the mother.

Animals↗
PubMed1988

[Milk ejection induced by PGF2 alpha during the first two months following insemination of cows. Application to pregnancy diagnosis].

Milk ejection after intrajugular injection of 256 micrograms of a synthetic PGF2 alpha analogue (Dinolytic, Upjohn) was measured every 2 days until D60 in 7 pregnant cows and until D25 in 5 non pregnant inseminated cows (trial 1). There was a very close correlation (r around + 0.98) between the values of the 3 parameters used to characterize milk ejection, i.e. amplitude of intramammary pressure deflection, surface area under the pressure curve, alveolar milk volume collected by a teat probe. In the two groups of animals, these values behaved similarly until D15 with a sudden increase between D2 and D7. From D15 they decreased abruptly in females where insemination had failed while they still remained at a high level until D25 (then decreasing until D60) in those presumed to be pregnant (fig. 2). These responses were assumed to result from the release of luteal oxytocin and it is suggested that a single injection of 256 micrograms of Dinolytic on D20, together with milk ejection control using a teat probe, would be a rapid, little expensive method for the farmer (without risks of luteolysis) (trial 2 and fig. 3) to distinguish between pregnant and non pregnant cows.

Animals↗
PubMed1998

[Failure of milk ejection reflex in primiparous cows from the differential diagnostic and therapeutic aspects].

A particular failure of the milk-ejection reflex in dairy cows is described on the base of own experiences in farms and reports from literature. Four cases are reported more in detail. Quantity and fat content of cisternal, alveolar and residual milk fractions, oxytocin content in blood serum, milk-ejection after manual teat stimulation, after massage of the clitoris or rectal stimulation of the vagina and cervix were investigated. This failure of the milk-ejection is observed mostly in primiparous cows and always at the begin of the lactation period. It is complete and permanent unless successfully treated, and seems to be based on an central inhibition of the oxytocin release. Treatment consists of thorough udder stimulation and milking followed by an i.v. application of oxytocin in order to remove the residual milk portion. The condition has a good prognosis, if the treatment is carried out regularly for some days and even weeks. Acute Mastitis is the main differential diagnosis.

Animals↗
PubMed1978

The milk ejection of the rat, as a stimulus and a response to the litter.

A finding that the milk ejection of the rat is stimulated effectively only if at least half the pups are suckled is confirmed. This relationship, however, is found if the mother is anaesthetized but not if the mother is conscious. If the mother is conscious, the milk obtained by individual hungry pups is unaffected by the number of other hungry pups suckled. This is true whether the other pups of the litter are removed, or whether they are present but satiated. After the milk ejection, pups tend to leave the mother's nipple. Milk yield decreases with each milk ejection of a series, but getting less milk does not make the pups more likely to leave the nipple in search of another.

Animal Population Groups↗
PubMed1975

Milk-ejecting and uterotonic activities of oxytocin analogues in rats.

The milk-ejecting activity of oxytocin analogues modified in the aminoterminal part of the molecule was determined in experiment on rats in vivo. As compared with oxytocin, the analogues did not have significantly higher milk-ejecting activity and there was no dissociation of the two basic oxytocin-like activities.

Animals↗
PubMed1979

Effect of prostaglandins on milk ejection.

Prostaglandins (PGs) of type F2 alpha, E1, and E2 have been reported both, to inhibit or to facilitate posterior pituitary oxytocin release in lactating animals and women, and to suppress or to stimulate the mammary myoepithelium. Prostaglandin-induced milk ejection in women and cows has been attributed to central oxytocin release, but no oxytocin blood levels were determined. Moreover, for lactating cows, sows, rabbits, guinea pigs, and rats a direct PG effect on the mammary myoepithelium resulting in milk ejection has been suggested. On the other hand, PGs were found to antagonize the milk-ejection response to oxytocin in rabbits and rats. The mechanisms involved in PG synergism or antagonism of oxytocin-induced milk ejection are not understood. Studies in lactating rats showed that blood pressure active PG doses of F2 alpha, E1, and E2 largely inhibited the intramammary pressure response to oxytocin. Whereas the oxytocin-antagonistic action of PGF2 alpha was not affected by adrenergic blockers (phenoxybenzamine, propranolol), the anti-oxytocin effects of PGE1 and E2 were eliminated after alpha-receptor blockade while the activity of oxytocin increased. Under beta-receptor or alpha- plus beta-receptor blockade, the oxytocin-inhibitory effects of PGE1 and E2 were almost abolished. Mechanisms of PG-induced inhibition of the oxytocin response may involve mammary vascular changes and/or alterations in myoepithelial activity of cyclic adenosine-3,5-monophosphate (c-AMP), cyclic guanosine-3,5-monophosphate (c-GMP), and phosphodiesterase (PDE). It seems unlikely that PGs bring about significant posterior pituitary oxytocin release in rats.

Animals↗
PubMed1993

Action of endogenous oxytocin within the paraventricular or supraoptic nuclei: a powerful link in the regulation of the bursting pattern of oxytocin neurons during the milk-ejection reflex in rats.

During suckling, the periodic and synchronous bursting activity of oxytocin neurons has been shown to be facilitated by oxytocin itself, acting via several target sites, including the magnocellular nuclei. To investigate the role of the endogenous oxytocin released within the magnocellular nuclei during the milk-ejection reflex in the rat, an oxytocin antagonist (50 microM solution of [d(CH2)5, Tyr(Me)2,Orn8]-vasotocin was pressure-injected into either one paraventricular or one supraoptic nucleus while recording the bursting pattern of oxytocin neurons within the injected nucleus and within a contralateral nucleus. The oxytocin antagonist was injected either during an ongoing milk-ejection reflex or during its facilitation induced by oxytocin (1 microliter of 1 microM solution injected into the third ventricle, i.e. 1 ng). During an ongoing milk-ejection reflex, injections of the oxytocin antagonist (10 nl of 50 microM solution, i.e. 50 ng) into the paraventricular or supraoptic nucleus decreased (more than 20% change) the burst amplitude (total number of spikes/burst) of neurons within the injected nucleus in 100% of tests, and simultaneously of contralateral neurons in 68% of tests. Burst periodicity of the entire population was also decreased in 50% of tests whatever the nucleus injected, but burst desynchronization was never observed. Successive injections of minute volumes of oxytocin (10 nl of 10 microM solution, i.e. 0.1 ng) into the paraventricular or supraoptic nucleus (which will progressively affect a greater number of neurons) first increased burst amplitude of oxytocin neurons within the injected nucleus and then increased simultaneously burst amplitude of contralateral neurons and burst frequency of the whole oxytocin neuron population. All these results suggest that the recruitment of a critical number of oxytocin neurons within one nucleus induces changes in the bursting activity of the oxytocin neurons in the four magnocellular nuclei. Within the minute following an intracerebroventricular oxytocin injection, the oxytocin antagonist injected into the supraoptic nucleus not only prevented the oxytocin-induced facilitation but also completely interrupted the milk-ejection reflex. When injected into the paraventricular nucleus, the oxytocin antagonist was less efficient: it decreased the oxytocin-induced facilitation but the reflex was not blocked. Similar partial inhibitory effect (decrease in burst amplitude and burst frequency) was also observed when the oxytocin antagonist was injected into the supraoptic nucleus after facilitation of the milk-ejection reflex by intracerebroventricular oxytocin injection. In conclusion, endogenous oxytocin released within the magnocellular nuclei during suckling represents a necessary link of the neuronal network regulating the bursting activity of oxytocin neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1961

Stress-induced block of milk ejection.

A simple method has been described by which the action of drugs on the stress-induced block in milk ejection can be investigated on lactating guinea-pigs. Reserpine, meprobamate and chlorpromazine when administered to the lactating mother at various periods before suckling reduced the block in milk ejection caused by the stress. Dibenamine and dichloroisoprenaline did not affect in any way the stress-induced block. It is suggested that the stress-induced block in milk ejection is probably a nervous block and not mediated through adrenaline.

Breast Feeding↗
PubMed1991

[The characteristics of the motor activity of rat pups during the milk ejection reflex].

The motor activity of newborn rats sucking on anesthetized mothers was studied during the milk ejection reflex. When sucking before obtaining milk every 22 +/- 12 sec, newborn rats displayed an increased motor activity which lasted for 5 +/- 3 sec and coincided with the period of high-amplitude fluctuations of the pressure exerted on the nipple. The periods (5-10 sec) of increased motor activity were observed simultaneously in two or more rats at intervals of 25-30 sec. Simultaneous activity of the newborn rats was most frequently observed 10-30 sec before reflex rise of milk pressure in the mammary gland. Factors regulating the milk ejection reflex in rats, are discussed.

Animals↗