EFFECT OF l-DOPA ON MILK EJECTION AND PROLACTIN RELEASE IN LACTATING RATS

1975 ◽  
Vol 67 (3) ◽  
pp. 397-401 ◽  
Author(s):  
J. PRILUSKY ◽  
R. P. DEIS
Keyword(s):  
Mammary Gland ◽  
Small Dose ◽  
Blocking Effect ◽  
Serum Prolactin ◽  
Nacl Solution ◽  
Suckling Period ◽  
Milk Ejection ◽  
Prolactin Release

SUMMARY The effect of l-DOPA on milk ejection and on prolactin release during 30 min of suckling was studied in lactating rats. Various doses of l-DOPA (1·25, 2·5, 5 and 10 mg/100 g body wt) were injected i.p. 30 min before the suckling period. Control rats were injected with 0·9% NaCl solution only. An inhibition of milk ejection proportional to the dose of drug administered was obtained. The dose of 10 mg completely blocked milk ejection but 1·25 mg had no effect. A normal milk-ejection response was obtained with a small dose of oxytocin injected immediately before nursing into mothers treated with 10 mg l-DOPA, indicating that the blocking effect was not due to a lack of mammary gland response. In control mothers, serum prolactin levels increased from 67·2 ± 25·9 (s.e.m.) to 950·3 ± 118·7 ng/ml after a 30 min suckling period. l-DOPA (5 and 10 mg) prevented the release of prolactin induced by suckling, but 1·25 and 2·5 mg l-DOPA had no effect. The results indicate that oxytocin and prolactin release induced by suckling in lactating rats is inhibited by an increase of catecholamines at the hypothalamic-hypophysial axis.

INHIBITORY EFFECT OF PROSTAGLANDIN F2α ON OXYTOCIN RELEASE AND ON MILK EJECTION IN LACTATING RATS

1976 ◽  
Vol 69 (3) ◽  
pp. 395-399 ◽  
Author(s):  
J. PRILUSKY ◽  
R. P. DEIS
Keyword(s):  
Mammary Gland ◽  
Prostaglandin F2α ◽  
Physiological Saline ◽  
Inhibitory Effect ◽  
Blocking Effect ◽  
Suckling Period ◽  
Milk Ejection ◽  
Oxytocin Release ◽  
Anaesthetized Rats ◽  
Prostaglandin F

SUMMARY The effect of prostaglandin F2α (PGF2α) on milk ejection and on oxytocin release during suckling for one or two periods of 30 min was studied in lactating rats. Doses of PGF2α (20 or 40 μg) 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 PGF2α, indicating that the blocking effect was not due to a lack of mammary gland response. Two groups of mothers were injected with 40 μg PGF2α 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, PGF2α (10 or 20 μg) did not modify the inhibition of milk ejection indicating that PGF2α 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 PGF2α, oxytocin was less effective. The results indicate that PGF2α 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.

EFFECT OF SUCKLING AND OF EXTEROCEPTIVE STIMULATION UPON PROLACTIN RELEASE IN THE RAT DURING LATE LACTATION

1972 ◽  
Vol 52 (1) ◽  
pp. 11-22 ◽  
Author(s):  
F. MENA ◽  
C. E. GROSVENOR
Keyword(s):  
Mammary Gland ◽  
Post Partum ◽  
Mammary Glands ◽  
The Other ◽  
Male Rats ◽  
Milk Secretion ◽  
Suckling Period ◽  
Prolactin Release ◽  
Other Hand ◽  
Rat Pituitary

SUMMARY The results of experiments in which the prolactin in the primiparous rat pituitary was bioassayed suggested that the failure of suckling to release prolactin after 8 h of non-suckling on day 21 post-partum was due to the fact that prolactin had been discharged from the pituitary during the 8-h non-suckling period, presumably by exteroceptive signals emanating from the general environment of the animal room. This was substantiated in other experiments in which prolactin release was assessed indirectly through its stimulatory effects upon milk secretion. In these experiments, the mammary glands of rats maintained continuously in the animal room filled faster on day 21 after complete emptying of the glands by exogenous oxytocin, than did either rats on day 14 post-partum maintained continuously in the animal room or rats isolated in a room without other rats on day 21 post-partum. The glands of the latter two groups of rats could be stimulated to fill faster provided prolactin was injected 4 h before the initial emptying of the glands. The exteroceptive stimuli in the animal room environment that stimulated the release of prolactin in the 21-day post-partum rat apparently emanated at least in part from other lactating rats and/or their litters, since faster mammary gland refilling occurred in isolated 21 day post-partum rats when they were exposed to the presence of lactating rats with their litters for 30 min halfway through the 8-h non-suckling period which preceded the initial emptying of the gland. Exposure to male rats, on the other hand, was totally ineffective. A release of prolactin occurred in response to animal room environmental stimuli in the day 14 primiparous rat provided 13–14 day old foster pups were inserted in place of the mother's own pups on day 7. Thus, the rapidly changing characteristics of the pups from 14 to 21 days of age in some manner is involved in the increasing responsiveness of the exteroceptive mechanism for prolactin release which occurs from day 14 to day 21 post-partum.

Stimulation of milk secretion with inhibition of milk ejection by corticosteroids during extended lactation in the rat

1984 ◽  
Vol 103 (2) ◽  
pp. 213-218 ◽  
Author(s):  
D. J. Flint ◽  
R. A. Clegg ◽  
C. H. Knight
Keyword(s):  
Adipose Tissue ◽  
Mammary Gland ◽  
Milk Yield ◽  
Insulin Receptors ◽  
Insulin Binding ◽  
Serum Prolactin ◽  
Milk Ejection ◽  
Anabolic Activity ◽  
Extended Lactation ◽  
Stimulation Of

ABSTRACT Milk yield declined significantly between days 22 and 28 of lactation in rats, when lactation was extended by frequent replacement of older litters with younger ones. Corticosterone implants but not cortisol injections or implants prevented this decline. Cortisol, however, appeared to inhibit milk ejection since the mammary glands became engorged with milk and milk yield was improved dramatically by oxytocin injections. In both cases corticosteroid concentrations increased approximately threefold above basal concentrations. Both corticosteroids increased total mammary gland RNA content and lipoprotein lipase (LPL) activity of the mammary gland but were without effect on insulin binding. They also decreased LPL activity, lipogenesis and the number of insulin receptors on adipose tissue. Serum prolactin and insulin concentrations were unaffected by any of the treatments. The results suggest that corticosteroids (1) inhibit milk ejection under certain conditions, (2) may be circulating in lower concentrations, which thereby limit milk production, during prolonged lactation and (3) may improve milk yield during extended lactation in part by suppressing anabolic activity in adipose tissue. J. Endocr. (1984) 103, 213–218

EFFECT OF LOCALLY IMPLANTED OESTROGEN ON THE RESPONSE OF THE RAT'S LACTATING MAMMARY GLAND TO OXYTOCIN

1973 ◽  
Vol 73 (4) ◽  
pp. 700-712 ◽  
Author(s):  
J. D. Bruce ◽  
X. Cofre ◽  
V. D. Ramirez
Keyword(s):  
Mammary Gland ◽  
Mammary Glands ◽  
Myoepithelial Cells ◽  
Recording System ◽  
Saline Infusion ◽  
High Dose ◽  
Low Doses ◽  
Milk Ejection ◽  
Lactating Mammary Gland ◽  
Small Rise

ABSTRACT On the day following delivery (day 1 of lactation) one abdominal mammary gland was implanted with oestrogen and the contralateral gland received an empty needle. At 2, 5 or 10 days of lactation the rats were anaesthetized with pentobarbital and the nipples of both abdominal glands were cannulated and their pressures recorded by means of transducers coupled to an amplifier and recording system. The normal mammary glands of 5-day lactating rats responded to very low doses of oxytocin (Syntocinon®, Sandoz) (5× 10−8 mU) with a rhythmic elevation in pressure. However, saline infusion also evoked a small rise in intra-mammary pressure. Earlier (2 days) and later (10 days) in lactation the responses were smaller. Oestrogen decreases significantly the milk ejection response to oxytocin, and the effect was maximal at day 10 of lactation. Histological observations confirmed the diminished reaction of the gland to oxytocin, since the milk was retained in the alveoli of rats bearing a mammary-oestrogen implant. A paradoxical rise in pressure was detected in normal as well as in oestrogen-implanted glands when the lowest dose of oxytocin was injected in lactating rats which had previously received a high dose of oxytocin (50 mU or 500 mU). These results reinforce the hypothesis that oestrogen alters the milk ejection response to oxytocin and that the mechanism is probably related to changes in the contractility of the myoepithelial cells.

INFLUENCE OF PHOTOPERIOD ON THYROTROPIN RELEASING HORMONE-INDUCED PROLACTIN RELEASE IN EWES

1983 ◽  
Vol 63 (1) ◽  
pp. 67-73 ◽  
Author(s):  
B. E. HOWLAND ◽  
D. SONYA ◽  
L. M. SANFORD ◽  
W. M. PALMER
Keyword(s):  
Thyrotropin Releasing Hormone ◽  
Day Length ◽  
Constant Light ◽  
Serum Prolactin ◽  
Prolactin Release ◽  
Blood Samples ◽  
Releasing Hormone ◽  
Before And After ◽  
Release Curve ◽  
Short Days

The influence of photoperiod on serum prolactin levels and prolactin release induced by thyrotropin releasing hormone (TRH) was determined in ewes maintained under the following lighting regimes: Room 1, lighting mimicked natural changes in photoperiod; Room 2, annual photoperiod changes condensed into 6 mo with short days in June; Room 3, same as Room 2 except photoperiod changed abruptly from 16.5 to 8.0 h on 21 Mar. and back to 16.5 h on 21 June; Room 4, constant light. Weekly blood samples were obtained from February to August. Additionally, blood samples were collected before and after treatment with 10 μg TRH on 19 May, 13 June, 27 June and 19 July. Prolactin levels were elevated in ewes exposed to long days or constant light. The mean of all pre-TRH samples was significantly correlated with stress-induced elevations in prolactin (highest pre-TRH value) (r = 0.72) and area under the TRH-induced release curve (r = 0.56). The prolactin release in response to TRH was greatest in ewes exposed to long days or constant light. Abrupt increase of day length elevated pretreatment prolactin levels (P < 0.01) and increased area under the response curve (P < 0.05). Key words: Photoperiod, TRH, prolactin, ewes

THE MOTILITY AND REACTIVITY OF THE OESTROGENIZED RABBIT UTERUS IN VIVO; WITH COMPARATIVE OBSERVATIONS ON MILK EJECTION

1958 ◽  
Vol 16 (3) ◽  
pp. 237-260 ◽  
Author(s):  
B. A. CROSS
Keyword(s):  
Spinal Cord ◽  
Mammary Gland ◽  
Spinal Anaesthesia ◽  
Dose Range ◽  
Abdominal Muscles ◽  
Mechanical Stimuli ◽  
Milk Ejection ◽  
Thoracic Spinal ◽  
Spontaneous Motility ◽  
Stimulation Of

SUMMARY The spontaneous motility of the intact uterus of spayed oestrogenized rabbits under sodium pentobarbitone anaesthesia has been recorded. Both uteri of each animal behaved similarly, and contractions often appeared to be synchronous. Small changes of load affected the amplitude of contractions, but did not alter uterine responsiveness to neurohypophysial or adrenomedullary hormones. Mid-thoracic section of the spinal cord obliterated spontaneous motility of the uterus; spinal anaesthesia did not. Spontaneous motility persisted for as long as 7 hr after decerebration and removal of the pituitary gland. The threshold dose of oxytocin for activating the oestrogenized uterus was the same as that for the lactating mammary gland, i.e. 1–5 mu. Doses up to 50 mu. usually gave an increase in frequency and amplitude of contractions. In the same dose range vasopressin either had little effect or inhibited spontaneous uterine motility, although milk ejection was stimulated. Slow infusion of oxytocin at rates of 1·5–48 mu./min produced graded increases in the rate and depth of uterine contractions and, at the same time, in similarly treated, lactating animals, rhythmic milk-ejection responses which at the higher rates of infusion merged to give a tetanic (plateau) type of milk ejection. Adrenaline or noradrenaline in doses of 1–5 μg produced diphasic uterine responses, initial contractions being followed by inhibition of spontaneous motility. They also inhibited the uterine, as well as the milk-ejection response to oxytocin injected 10–30 sec later. The inhibitory effect of adrenaline on both organs was about twice that of noradrenaline. The above-mentioned responses to adrenaline and oxytocin could also be elicited by electrical stimulation of the hypothalamus. Stimuli in the dorsal, lateral, perifornical and posterior hypothalamic areas produced effects equivalent to those of 1–5 μg adrenaline on both the uterus and mammary gland. These responses were abolished by mid-thoracic section of the spinal cord or by spinal anaesthesia. In such preparations responses typical of those produced by oxytocin were seen in both organs after stimulation of the paraventricular nuclei, supraoptic nuclei and the hypothalamo-hypophysial nerve pathways of the tuber cinereum and neural stalk. Dilatation of the vagina (or rectum) gave rise to a uterine response similar to that resulting from adrenaline or noradrenaline. The response was abolished by spinal anaesthesia, but not by mid-thoracic spinal section or decerebration. The same stimuli also produced 'bearing down' contractions of the abdominal muscles. Contractions of the uterus could also be elicited by mechanical stimuli, in the absence of functional spinal connexions.

scholarly journals Growth-hormone-prolactin interactions in the regulation of mammary and adipose-tissue acetyl-CoA carboxylase activity and gene expression in lactating rats

1992 ◽  
Vol 285 (2) ◽  
pp. 469-475 ◽  
Author(s):  
M C Barber ◽  
M T Travers ◽  
E Finley ◽  
D J Flint ◽  
R G Vernon
Keyword(s):  
Adipose Tissue ◽  
Mammary Gland ◽  
Serum Prolactin ◽  
Acetyl Coa Carboxylase ◽  
Acetyl Coa ◽  
Carboxylase Activity ◽  
Total Enzyme Activity ◽  
Mrna Concentration ◽  
Total Enzyme ◽  
Activation Status

The factors and mechanisms responsible for the reciprocal changes in lipogenesis in rat mammary gland and adipose tissue during the lactation cycle have been investigated. Lactation decreased the activation status and mRNA concentration of acetyl-CoA carboxylase in adipose tissue. Litter removal decreased the mRNA concentration of acetyl-CoA carboxylase in the mammary gland and increased the enzyme's mRNA concentration and activation status in adipose tissue. Lowering serum prolactin concentration in lactating rats decreased the amount of mammary acetyl-CoA carboxylase mRNA and increased that of adipose tissue, and increased the activation status of the enzyme in adipose tissue. Decreasing serum growth hormone (GH) alone had little effect on acetyl-CoA carboxylase in lactating rats, although it did lower pup growth rate and serum concentration of insulin-like growth factor-I. Lowering serum GH concentration exacerbated the effects of decreasing serum prolactin on mammary-gland (but not adipose-tissue) acetyl-CoA carboxylase mRNA and further increased the rise in activation status of the adipose-tissue enzyme induced by decreasing serum prolactin. Changes in acetyl-CoA carboxylase mRNA in both mammary and adipose tissue were paralleled by changes in total enzyme activity except after litter removal, when there was a disproportionately large decrease in total enzyme activity of the mammary gland. Thus prolactin has a major and GH a minor role in the regulation of acetyl-CoA carboxylase activity during lactation. Changes in mammary activity in response to prolactin and GH are primarily due to alterations in gene transcription, whereas adaptation in adipose tissue involves both changes in gene transcription and activation status.

Prolactin release, oestrogens and proliferation of prolactin-secreting cells in the anterior pituitary gland of adult male rats

1986 ◽  
Vol 108 (3) ◽  
pp. 399-403 ◽  
Author(s):  
R. L. Pérez ◽  
G. A. Machiavelli ◽  
M. I. Romano ◽  
J. A. Burdman
Keyword(s):  
Cell Proliferation ◽  
Pituitary Gland ◽  
Adult Male ◽  
Anterior Pituitary ◽  
Pituitary Hormones ◽  
Anterior Pituitary Gland ◽  
Male Rats ◽  
Serum Prolactin ◽  
Prolactin Release ◽  
Experimental Conditions

ABSTRACT Relationships among the release of prolactin, the effect of oestrogens and the proliferation of prolactin-secreting cells were studied under several experimental conditions. Administration of sulpiride or oestradiol released prolactin and stimulated cell proliferation in the anterior pituitary gland of adult male rats. Clomiphene completely abolished the rise in cell proliferation, but did not interfere with the sulpiride-induced release of prolactin. Treatment with oestradiol plus sulpiride significantly increased serum prolactin concentrations and the mitotic index compared with the sum of the stimulation produced by both drugs separately. Bromocriptine abolished the stimulatory effect of oestradiol on the serum prolactin concentration and on cell proliferation. In oestradiol- and/or sulpiride-treated rats, 80% of the cells in mitoses were lactotrophs. The remaining 20% did not stain with antisera against any of the pituitary hormones. The number of prolactin-secreting cells in the anterior pituitary gland significantly increased after the administration of oestradiol or sulpiride. The results demonstrate that treatment with sulpiride and/or oestradiol increases the proliferation and the number of lactotrophs in the anterior pituitary gland of the rat. J. Endocr. (1986) 108, 399–403

Effect of Various Hormones on the Milk Ejection Response of Tissue isolated from the Rat Mammary Gland

Nature ◽  
1967 ◽  
Vol 213 (5076) ◽  
pp. 632-633 ◽  
Author(s):  
C. G. VAN DONGEN ◽  
J. M. MARSHALL
Keyword(s):  
Mammary Gland ◽  
Milk Ejection ◽  
Rat Mammary Gland
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