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.

ETHANOL AND THE INHIBITION OF OXYTOCIN RELEASE IN LACTATING RATS

1969 ◽  
Vol 62 (3) ◽  
pp. 546-554 ◽  
Author(s):  
Anna-Riitta Fuchs
Keyword(s):  
Mammary Gland ◽  
Dose Level ◽  
Milk Yield ◽  
Complete Inhibition ◽  
Milk Ejection ◽  
Oxytocin Release ◽  
Anaesthetized Rats ◽  
Peripheral Effect ◽  
Higher Doses

ABSTRACT The effect of ethanol on the release of oxytocin in the rat was studied using suckling as the oxytocin releasing stimulus. Milk removal on 30 min suckling by a litter of 8 after 18 h separation from the mother on postpartum day 13–16 was used as a parameter of oxytocin liberation. Under these conditions 25 mU intravenously injected oxytocin permitted normal milk removal in anaesthetized rats, whereas after injection of 10 mU oxytocin only about half of the normal milk yield was obtained. Ethanol in doses varying from 1.0 to 5.0 g/kg was injected intraperitoneally into the dam as 10 to 20 % solution in saline 30 to 60 min before nursing commenced and the milk yield was compared with saline injected control rats. At the dose level of 1.0 g/kg ethanol had no effect on milk removal but 2.0 g/kg caused a significant reduction to about 60 % of normal, and with higher doses a further reduction of the milk yield occurred. At 3.5 g/kg about 14% of normal milk yield was obtained, and at 5.0 g/kg a complete inhibition of milk ejection was observed. Oxytocin administration permitted normal milk removal in all ethanol treated rats indicating that there was no peripheral effect on the mammary gland. The experiments suggest that ethanol inhibits oxytocin release also in the rat.

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.

scholarly journals Effects of benzene, quercetin, and their combination on porcine ovarian cell proliferation, apoptosis, and hormone release

2019 ◽  
Vol 62 (1) ◽  
pp. 345-351 ◽  
Author(s):  
Adam Tarko ◽  
Aneta Štochmal'ová ◽  
Katarína Jedličková ◽  
Sandra Hrabovszká ◽  
Adriana Vachanová ◽  
...  
Keyword(s):  
Granulosa Cell ◽  
Protective Action ◽  
Inhibitory Effect ◽  
Hormone Release ◽  
Ovarian Cell ◽  
Cell Functions ◽  
Ovarian Granulosa Cell ◽  
Oxytocin Release ◽  
Prostaglandin F

Abstract. We hypothesized that the environmental contaminant benzene and the plant antioxidant quercetin may affect ovarian cell functions and that quercetin could offer protection against the adverse effects of benzene. This study aimed to examine the action of benzene, quercetin, and their combination on porcine ovarian granulosa cell functions. We elucidated the effects of benzene (20 µg mL−1), quercetin (at the doses 0, 1, 10, 100 µg mL−1), and their combination on ovarian granulosa cell functions (proliferation, apoptosis, and hormone release) in vitro using immunocytochemistry and enzyme immunoassay respectively. Benzene alone stimulated proliferation, apoptosis, and oxytocin release and inhibited progesterone and prostaglandin F release. Quercetin alone inhibited proliferation, apoptosis, and stimulated oxytocin release but did not affect progesterone and prostaglandin F release. When used in combination with benzene, quercetin promoted the inhibitory effect of benzene on progesterone release. Overall, these data suggest that benzene and quercetin have direct stimulatory and inhibitory effects, respectively, on basic ovarian functions. Moreover, no protective action of quercetin against the effects of benzene was found. Rather, it was found to enhance the effect of benzene on progesterone release. Therefore, quercetin cannot be considered for preventing or mitigating the effects of benzene on reproductive processes.

FAILURE OF EXOGENOUS PROSTAGLANDIN F2α TO ENHANCE UTERINE INVOLUTION IN BEEF COWS

1988 ◽  
Vol 68 (3) ◽  
pp. 669-676 ◽  
Author(s):  
L. A. GUILBAULT ◽  
P. VILLENEUVE ◽  
J. J. DUFOUR
Keyword(s):  
Plasma Concentrations ◽  
Prostaglandin F2α ◽  
Physiological Saline ◽  
Beef Cows ◽  
Tissue Loss ◽  
Primary Metabolite ◽  
Descending Aorta ◽  
Uterine Involution ◽  
Prostaglandin F ◽  
Calf Removal

Twenty-four beef cows of 5th parity were fitted with catheters in the descending aorta via a superficial costoabdominal artery. On the day of parturition (day 0), cows were assigned randomly and equally to two infusion treatments and three slaughter groups. Cows were infused continuously for 11 d with either prostaglandin F2α-tham salt (PGF2α; 33.5 mg d−1 from days 2 to 13) or 0.9% physiological saline (saline) via the descending aorta. In the first slaughter group, cows were suckled until slaughtered on day 15. Cows in the second slaughter group were suckled until slaughtered on day 35; whereas in the third group, calves were weaned on day 31 and cows slaughtered on day 35. Reproductive tracts were collected at slaughter and degree of uterine involution was assessed by recording weight and diameter of the cervix, weight, diameter and length of both uterine horns as well as surface areas of caruncular and intercaruncular endometrium. During the infusion period, plasma concentrations of 15-keto-13, 14-dihydro-PGF2α, the primary metabolite of PGF2α, were higher in PGF2α- than in saline-infused cows (1091 vs 738 pg mL−1, SE = 105, P < 0.03). All cervical and uterine (except uterine horn diameter) measures of involution were greater (P < 0.1) on day 15 than on day 35. Calf removal did not affect (P > 0.1) uterine involution on day 35. None of the responses measured to assess uterine involution differed (P > 0.1) between PGF2α- and saline-infused cows on day 15 or 35. It is concluded that early postpartum administration of PGF2α by continuous infusion does not alter uterine involution in terms of reduction in size and tissue loss by days 15 and 35 postpartum. Key words: Cows, postpartum, prostaglandin F2α, uterine involution.

ELECTROPHYSIOLOGICAL RECORDINGS FROM OXYTOCINERGIC NEURONES DURING SUCKLING IN THE UNANAESTHETIZED LACTATING RAT

1981 ◽  
Vol 90 (2) ◽  
pp. 255-265 ◽  
Author(s):  
A. J. S. SUMMERLEE ◽  
D. W. LINCOLN
Keyword(s):  
High Frequency ◽  
Action Potentials ◽  
Milk Ejection ◽  
Extracellular Recordings ◽  
Electrophysiological Recordings ◽  
Oxytocin Release ◽  
Anaesthetized Rats ◽  
Freely Moving ◽  
Frequency Burst ◽  
Stimulation Of

A method is described for making extracellular recordings of the spontaneous activity of single hypothalamic neurones in unanaesthetized, freely moving, lactating rats using chronically implanted micro-wire electrodes. Extracellular recordings taken from individual neurones were maintained for periods of between 1 and 12 days. These records were not affected by any normal movement of the animal. As several micro-wires were implanted into each animal it was possible to make simultaneous recordings from several different hypothalamic sites in the same animal. Some recordings were identified as those from magnocellular neurones in the paraventricular nucleus on the basis of antidromic invasion after electrical stimulation of the neurohypophysis. Milk ejection in response to the prolonged sucking of ten or more pups was intermittent, and individual milk ejections recurred at intervals of 2–10 min throughout each period of nursing. The rise in intramammary pressure at milk ejection was associated with a vigorous extensor response from the pups. This was monitored by radar to provide an index of milk ejection in the unanaesthetized rat. Eleven antidromically identified neurones were recorded through 321 milk ejections. Eight of these neurones displayed a transient (2–6 s) and very substantial acceleration in discharge at the time predicted for oxytocin release, i.e. 10–12 s before milk ejection. The background discharge of these cells was 0·1–2·6 action potentials/s; this increased to 16–50 action potentials/s during the brief period of accelerated activity. Twenty-five neurones were studied during 365 milk ejections in rats which did not have a stimulating electrode implanted in the neurohypophysis. Thirteen of these neurones displayed a burst of high frequency discharge before each milk ejection, similar to that described for the antidromically identified neurones. Two of the non-responsive cells displayed a phasic pattern of discharge, characteristic of vasopressinergic neurone discharge recorded in anaesthetized rats. These observations of putative oxytocinergic neurones in unanaesthetized, freely moving rats are identical with those previously made on anaesthetized rats, and establish that the high frequency burst of electrical activity displayed by magnocellular neurones some 10–12 s before milk ejection is responsible for oxytocin release under normal physiological circumstances.

Influence of cerebral cortex in inhibition of oxytocin release induced by stressful stimuli

1964 ◽  
Vol 207 (6) ◽  
pp. 1394-1398 ◽  
Author(s):  
S. Taleisnik ◽  
R. P. Deis
Keyword(s):  
Cerebral Cortex ◽  
Cortical Spreading Depression ◽  
Inhibitory Action ◽  
Spreading Depression ◽  
Marked Decrease ◽  
Mammary Glands ◽  
Inhibitory Effect ◽  
Milk Ejection ◽  
Oxytocin Release ◽  
Central Inhibition

Weight increase of a litter of rats during the course of 1 hr of suckling, after a 9-hr separation from their mothers, was taken as a measure of the amount of oxytocin released. The opening in the mother of an orifice in the cranium, on each side of the midline (bilateral trauma), or the fracture of one femur (unilateral trauma) caused a marked decrease in the litter's weight gain. Milk ejection so depressed was restored to the normal level by administration of oxytocin (20 mU/100 g). Stimuli arising from the traumatized area, therefore, exert a central inhibition on oxytocin release. In hemimammectomized animals, femoral fracture on the side with intact mammary glands has a greater inhibitory effect than the fracture on the opposite side. Topical application of 25% KCl on the cerebral cortex, in order to induce cortical spreading depression, caused the disappearance of the inhibition of oxytocin secretion. The influence of corticofugal systems on the reticular formation as a possible mechanism responsible for the suppression of the inhibitory action of stimuli on the release of oxytocin is discussed.

Prostaglandin F2α and oxytocin release during persistence of the corpus luteum in sheep

1987 ◽  
Vol 115 (4) ◽  
pp. 469-477 ◽  
Author(s):  
S. B. Hooper ◽  
G. D. Thorburn
Keyword(s):  
Corpus Luteum ◽  
Prostaglandin F2α ◽  
Pulse Frequency ◽  
Ovarian Vein ◽  
Luteal Regression ◽  
Oxytocin Release ◽  
Prostaglandin F ◽  
Frequency Of Stimulation

Abstract. Oxytocin (OT), progesterone and prostaglandin F2α (PGF2α) concentrations were measured in the utero-ovarian vein (UOV) of ewes which displayed persistence of the corpus luteum (CL). During the period of expected luteolysis, the frequency of OT and PGF2α pulses in the UOV was significantly (P < 0.005 for both) lower in ewes with persistent CLs, compared with ewes that underwent normal luteal regression. In contrast, the amplitude of both OT and PGF2α pulses was similar in both groups of animals. It is suggested that persistence of the CL resulted from a decreased PGF2α pulse frequency, which may have arisen from a decreased frequency of stimulation by OT. In two persistent CL ewes, however, it appeared that a failure at the level of the uterus may have contributed to the observed decrease in PGF2α release. Although a PGF2α analogue (Lutalyse) infusion into the uterine vein of two ewes with persistent CLs failed to induced luteolysis, it did stimulate a large release of OT into the UOV. This suggests that persistent CLs maybe more resistant to PGF2α and, that at day 22 post-oestrus, these CLs are capable of releasing large quantities of OT into the UOV.

Potential role for lipoxygenase products of arachidonic acid in prostaglandin F2α-stimulated oxytocin release from the ovine corpus luteum

1994 ◽  
Vol 142 (1) ◽  
pp. 47-52 ◽  
Author(s):  
R G Cooke ◽  
N Ahmad
Keyword(s):  
Arachidonic Acid ◽  
Corpus Luteum ◽  
Potential Role ◽  
Prostaglandin F2α ◽  
Nordihydroguaiaretic Acid ◽  
Luteal Function ◽  
Lipoxygenase Inhibition ◽  
Lipoxygenase Products ◽  
Oxytocin Release ◽  
Prostaglandin F

Abstract Intrauterine administration of nordihydroguaiaretic acid (NDGA) will maintain luteal function in sheep and also suppress the release of both oxytocin and prostaglandin F2α (PGF2α) suggesting that 5-lipoxygenase products of arachidonic acid may be involved in ovine luteolysis. During luteolysis, uterine PGF2α is considered to be the major stimulus for the secretion of luteal oxytocin, and we report the effects of 5-lipoxygenase inhibition, via intrauterine NDGA administration, on the ability of PGF2α to effect such secretion. In the NDGA-treated ewes, luteal function was maintained and oestrus delayed, the duration of the oestrous cycle (20 ±1 days; mean ± s.d.; n=9) being significantly (P<0·01) longer than in intact controls (15 ± 1 days, n=4). Jugular infusions of PGF2α did not stimulate luteal secretion of oxytocin, the effects being comparable with those in ovariectomized ewes. In intact ewes receiving intrauterine infusions of vehicle only, PGF2α produced marked increases in luteal secretion of oxytocin. Also, preinfusion or basal concentrations of oxytocin in this group of ewes (6·6 ± 1·9 pg/ml) were significantly (P<0·01) greater than in either the NDGA-treated (3·1 ± 1·1 pg/ml) or ovariectomized (3·0 ± 0·6 pg/ml) ewes. The results suggest involvement of 5-lipoxygenase products of arachidonic acid in the release of oxytocin from the ovine corpus luteum. Journal of Endocrinology (1994) 142, 47–52

Agonists of endogenous opioid peptides suppress LH, and stimulate cortisol and growth hormone during the follicular phase in heifers

1989 ◽  
Vol 121 (1) ◽  
pp. 11-17 ◽  
Author(s):  
J. D. Armstrong ◽  
B. H. Johnson
Keyword(s):  
Opioid Receptor ◽  
Physiological Saline ◽  
Inhibitory Effect ◽  
Follicular Phase ◽  
Endogenous Opioid ◽  
Receptor Agonists ◽  
Prostaglandin F ◽  
Induced Changes ◽  
Opioid Receptor Agonists ◽  
Angus Heifers

ABSTRACT We evaluated the effects of [d-Ala2,Me,Phe4,Met(0)ol]-enkephalin (FK 33-824) and morphine, opioid receptor agonists, on concentrations of LH, cortisol and GH during the follicular phase in heifers. During three trials, oestrous cycles of Angus heifers were synchronized by two injections of prostaglandin F2α (PGF2α) resulting in 17 induced follicular phases over an 80-day period. Treatments were administered 24 h after the second injection of PGF2α. Blood samples were collected at 15-min intervals from 3 h before until 5 h after i.v. administration of 2 ml physiological saline (trials 1, 2 and 3), 0·5 mg morphine/kg (trials 1 and 2) or 1·8 μg FK 33-824/kg (trials 1 and 2) or 6·7 μg FK 33-824/kg (trial 3). Administration of both doses of FK 33-824 and morphine inhibited episodic release of LH for approximately 60 min. The concentration of cortisol was increased (P<0·05) after both doses of FK 33-824, but was unaffected (P>0·5) by morphine or saline. The serum concentration of GH was increased (P<0·01) after both doses of FK 33-824 or morphine, but saline was without effect. These results provide evidence of an inhibitory effect of opioid receptor agonists on LH (FK 33-824 and morphine) and a stimulatory effect on cortisol (FK 33-824) and GH (FK 33-824 and morphine) during the follicular phase in heifers. Divergent effects of morphine and FK 33-824 on cortisol observed in this study provide evidence that opioid-induced changes in LH, GH and cortisol result from activation of different opioid receptors. Journal of Endocrinology (1989) 121, 11–17

INHIBITORY EFFECT OF PROGESTERONE ON THE LACTOGENIC AND ABORTIVE ACTION OF PROSTAGLANDIN F2α

1975 ◽  
Vol 66 (1) ◽  
pp. 21-29 ◽  
Author(s):  
NELIA T. VERMOUTH ◽  
R. P. DEIS
Keyword(s):  
Single Dose ◽  
Plasma Concentration ◽  
Prostaglandin F2α ◽  
Inhibitory Effect ◽  
Induced Abortion ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Pregnant Rats ◽  
Unilateral Ovariectomy ◽  
Prostaglandin F

SUMMARY The effect of ovariectomy, progesterone and prolactin treatment on the action of prostaglandin F2α (PGF2α) was determined in pregnant rats. PGF2α (150 μg × 2) injected i.p. on day 19 or 18 of pregnancy induced lactogenesis about 25 h later and abortion on days 20 and 21 of pregnancy. Treatment with PGF2α (100 μg × 2 or 50 μg × 2) on day 19 induced lactogenesis around 22 or 38 h later, respectively, and abortion on day 21. PGF2α treatment on day 17 was less effective. Unilateral ovariectomy on day 17 of pregnancy induced lactogenesis 32 h later but not abortion. PGF2α (150 μg × 2) given on the day of surgery advanced lactogenesis 12 h and rats aborted on day 19. Bilateral ovariectomy on day 17 induced abortion between days 20 to 21, but if a single dose of PGF2α (300 μg) was injected on day 18, all the ovariectomized rats aborted on day 19. Progesterone (10 mg) injected into rats treated with PGF2α (150 μg × 2) on day 18, prevented abortion and delayed lactogenesis. Prolactin (1 mg × 4) treatment delayed only abortion. Serum prolactin levels were significantly higher 12 h after the last dose of PGF2α (150 μg × 2) in rats treated on days 17, 18 or 19 of pregnancy. Pretreatment with progesterone prevented the rise in prolactin concentration. These results suggest that the lactogenic and abortive action of PGF2α may be dependent on the uterine and plasma concentration of progesterone.

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