FAILURE OF MELATONIN TO INCREASE SERUM PROLACTIN LEVELS IN OVARIECTOMIZED RATS SUBJECTED TO SUPERIOR CERVICAL GANGLIONECTOMY OR PINEALECTOMY

1979 ◽  
Vol 82 (2) ◽  
pp. 315-319 ◽  
Author(s):  
D. P. CARDINALI ◽  
MARÍA R. FAIGÓN ◽  
P. SCACCHI ◽  
J. MOGUILEVSKY
Keyword(s):  
Pineal Gland ◽  
Steroid Treatment ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Prolactin Release ◽  
Intracranial Surgery ◽  
Superior Cervical Ganglionectomy ◽  
Significant Depression

SUMMARY The effects of melatonin on serum prolactin levels were examined in ovariectomized rats primed with oestradiol and progesterone, and subjected to bilateral superior cervical ganglionectomy or pinealectomy. Ganglionectomy resulted in a significant depression of the serum prolactin concentration, as well as in impairment of the prolactin release evoked by administration of steroid. Treatment with melatonin increased serum prolactin in control but not in ganglionectomized rats. Injection of melatonin potentiated the steroid-induced release of prolactin in control rats; this effect of melatonin was not detected in ganglionectomized rats. Pinealectomy did not affect basal prolactin levels, nor impair the release of prolactin evoked by steroid treatment; however, it was effective in blocking the melatonin-induced release of prolactin in vehicletreated rats, as well as the potentiation of steroid-induced prolactin release by melatonin. Intracranial surgery by itself increased prolactin release. These results suggest that systemically administered melatonin needs an intact pineal gland to augment serum prolactin levels.

FEEDBACK EFFECTS OF STEROIDS ON GONADOTROPHIN RELEASE IN HYPERPROLACTINAEMIC, OVARIECTOMIZED RATS

1981 ◽  
Vol 89 (3) ◽  
pp. 431-435 ◽  
Author(s):  
D. A. CARTER ◽  
S. A. WHITEHEAD
Keyword(s):  
Direct Action ◽  
Steroid Treatment ◽  
Ovariectomized Rats ◽  
Prolactin Release ◽  
Feedback Effects ◽  
Lh Surge ◽  
Kidney Capsule ◽  
Pituitary Glands ◽  
Hypothalamic Pituitary Axis

The effect of hyperprolactinaemia on the progesterone-induced LH surge which occurs in oestrogen-primed, ovariectomized rats has been investigated. Hyperprolactinaemia was produced by implanting pituitary glands under the kidney capsule and levels of LH and prolactin in the circulation were measured at appropriate times during the steroid treatment. Twenty-four hours after oestrogen administration plasma LH levels were significantly reduced in both hyperprolactinaemic and sham-operated control rats. Progesterone induced a surge of LH which peaked 5 h after injection in both groups of rats. However, the peak LH level in the hyperprolactinaemic rats was less than 50% of that observed in the controls. Differences were also found in the effect of oestrogen on prolactin release in the hyperprolactinaemic rats. It is suggested that prolactin reduces the sensitivity to progesterone by a direct action on the hypothalamic–pituitary axis.

INVOLVEMENT OF NEURONES CONTAINING 5-HYDROXYTRYPTAMINE IN THE MECHANISM OF PROLACTIN RELEASE INDUCED BY OESTROGEN

1974 ◽  
Vol 62 (1) ◽  
pp. 25-33 ◽  
Author(s):  
L. CALIGARIS ◽  
S. TALEISNIK
Keyword(s):  
Third Ventricle ◽  
Steroid Treatment ◽  
Serum Prolactin ◽  
Prolactin Release ◽  
Thyrotrophin Releasing Hormone ◽  
Ovarian Steroids ◽  
Neuronal Mechanism ◽  
The Third ◽  
Oestradiol Benzoate ◽  
The Brain

SUMMARY Oestradiol benzoate (OB) injected into spayed rats induced high levels of serum prolactin (measured by radioimmunoassay) in the afternoon of the third day after the injection. When progesterone was injected into spayed rats primed 3 days before with OB, a release of prolactin was observed in the morning. These rises in serum prolactin were prevented either by treatment with p-chlorophenylalanine (PCPA), a compound which depletes 5-hydroxytryptamine (5-HT) from the brain or by injecting the 5-HT antagonist methysergide, into the third ventricle. The blockade of prolactin release by PCPA treatment of OB-injected rats was partially reversed by the administration of 5-hydroxytryptophan. These results indicate that 5-HT containing neurones mediate the effect of ovarian steroids on prolactin release. Further support of this view was provided by experiments showing that the injection of 5-HT into the third ventricle raised serum prolactin levels. The rise in serum prolactin observed after the ovarian steroid treatment was blocked to a great extent by the injection of picrotoxin or strychnine. Picrotoxin also blocked the rise in serum prolactin induced by the injection of 5-HT into the third ventricle but failed to affect the rise in serum prolactin after i.v. injection of thyrotrophin-releasing hormone or α-methyl-p-tyrosine treatment. The results suggest that an inhibitory neuronal mechanism mediated by 5-HT neurones is involved in the release of prolactin induced by ovarian steroids.

EFFECTS OF PINEALECTOMY ON THE RAT OESTROUS CYCLE AND PITUITARY GONADOTROPHIN RELEASE

1976 ◽  
Vol 69 (1) ◽  
pp. 67-75 ◽  
Author(s):  
C. A. BLAKE
Keyword(s):  
Pineal Gland ◽  
Oestrous Cycle ◽  
Ovariectomized Rats ◽  
Prolactin Release ◽  
Medial Basal Hypothalamus ◽  
Blood Samples ◽  
Serum Lh ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Permissive Role

SUMMARY In 4-day cyclic rats kept in a room with the lights on from 05.00 to 19.00 h, sham pinealectomy or pinealectomy on the morning of pro-oestrus did not alter the length of the oestrous cycle for 44 days or the time and magnitude of the rises in LH, FSH and prolactin in the circulation in the afternoon on pro-oestrous days 0, 20 or 44. On day 45, the light schedule was set forward 4 h to run from 09.00 to 23.00 h. The rats continued to have seven additional consecutive 4-day oestrous cycles. On day 27 after the resetting of the light schedule, the pro-oestrous rises in serum LH, FSH and prolactin were delayed 4 h in all rats and a normal quota of eggs was ovulated that night. Other 4- and 5-day cyclic rats which had been made persistently oestrous by anterior deafferentation of the medial basal hypothalamus (AC) underwent pinealectomy. These AC-pinealectomized rats were ovariectomized 60 days later and histological examination of the ovaries revealed no evidence of recent ovulation. Five to six weeks after ovariectomy, sequential blood samples were withdrawn through indwelling atrial cannulas in the AC-pinealectomized-ovariectomized rats and in ovariectomized, pinealectomized-ovariectomized and AC-ovariectomized rats. Regular pulsatile rhythms in plasma LH were measured in all rats. Subcutaneous injection of 50 μg oestradiol benzoate in oil lowered plasma LH levels in all four groups but caused an LH surge in the afternoon 2 days later only in the ovariectomized and pinealectomized-ovariectomized rats. The results indicate that the pineal gland in rats kept on a 14 h light: 10 h darkness schedule does not play an active or permissive role in the timing or magnitude of LH, FSH or prolactin release at pro-oestrus, the length of the oestrous cycle, or LH release in ovariectomized rats.

PROLACTIN RELEASE AND LACTOGENESIS AFTER OVARIECTOMY IN PREGNANT RATS: EFFECT OF OVARIAN HORMONES

1974 ◽  
Vol 63 (1) ◽  
pp. 13-20 ◽  
Author(s):  
NELIA T. VERMOUTH ◽  
R. P. DEIS
Keyword(s):  
Ovarian Hormones ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Rapid Rise ◽  
Prolactin Release ◽  
Pregnant Rats ◽  
Blood Concentrations ◽  
Oestrogen Treatment ◽  
Progesterone Treatment

SUMMARY Ovariectomy of rats on day 19 of pregnancy induced a rapid rise in serum prolactin. Levels were significantly increased 4 h after removal of the ovaries and continued to rise up to 24 h. A transient fall occurred at 32 h, but serum prolactin concentration was still raised after 36, 48 and 58 h. Similar increases of serum prolactin occurred after ovariectomy on days 17 and 18 of pregnancy. Lactogenesis occurred 24·8 or 28·2 h after ovariectomy on days 19 or 17–18 of pregnancy respectively. Rats ovariectomized on day 17 or 18 delivered on day 21 and rats ovariectomized on day 19 delivered on day 22 of pregnancy. Ovariectomy impaired parturition in all groups. Treatment with oestrogen immediately after the operation did not prevent the rise in serum prolactin levels 4, 8 and 12 h after ovariectomy, but 24 h after ovariectomy, prolactin values were not significantly different from those in sham-operated control rats. When oestrogen was injected 12 h after ovariectomy, serum prolactin was markedly increased 12 h later. Lactogenesis occurred about 22·9 h after oestrogen treatment and all animals delivered on day 21 of pregnancy. Progesterone treatment prevented the rise in prolactin levels observed 4 and 8 h after ovariectomy, but at 12 h levels had risen and were similar to those observed in untreated ovariectomized rats. Progesterone prevented lactogenesis for 14 h (around 37.5 h after ovariectomy) and induced a delay in the onset of parturition. The results indicate that the decrease of progesterone in the blood after ovariectomy in pregnant rats may induce a release of prolactin and lactogenesis. Oestrogen seems to be effective in raising prolactin levels at low blood concentrations of progesterone.

A possible dual regulation of prolactin release by the serotoninergic system in rats at pro-oestrus and during late pregnancy: role of ovarian hormones

1987 ◽  
Vol 112 (3) ◽  
pp. 367-374 ◽  
Author(s):  
G. A. Jahn ◽  
R. P. Deis
Keyword(s):  
Serotonin Receptor ◽  
Late Pregnancy ◽  
Inhibitory Effect ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Serotoninergic System ◽  
Serum Concentrations ◽  
Prolactin Release ◽  
Treatment Administration ◽  
Significant Release

ABSTRACT The effect of para-chlorophenylalanine (pCPA), an inhibitor of serotonin synthesis, on prolactin release was studied in rats on the day of pro-oestrus and at the end of pregnancy (day 19). The surges of prolactin normally seen in the afternoon of pro-oestrus in intact rats and in rats ovariectomized on dioestrous day 2 and primed with oestrogen were significantly inhibited by pCPA treatment. Administration of 5-hydroxy-tryptophan reversed the inhibitory action of pCPA on prolactin release. Treatment with progesterone also completely reversed the inhibitory effect of pCPA on prolactin release in pro-oestrous rats and partially reversed it in ovariectomized oestrogen-treated rats. Ovariectomy on day 19 of pregnancy induced a significant release of prolactin 12 and 24 h later. Administration of pCPA on day 18 of pregnancy produced a marked increase in serum concentrations of prolactin on days 19 and 20 in rats left intact or ovariectomized on day 19. Administration of 5-hydroxy-tryptophan significantly reversed this stimulatory effect of pCPA on prolactin release but did not modify the release of prolactin induced by ovariectomy. Methiothepin (1-[10,11-dihydro-8-(methylthio) <b,f> thiepin-10,41]-4-methylpiperazine maleate), a serotonin receptor blocker, also induced a significant increase in serum concentrations of prolactin on day 20 of pregnancy in rats left intact or ovariectomized on day 19. These results suggest the existence of different serotoninergic actions in the regulation of prolactin release at pro-oestrus and in late pregnancy. Serotonin facilitates the surges of serum prolactin released at pro-oestrus and in ovariectomized rats treated with oestrogen; progesterone enhances this effect. On the other hand, during late pregnancy, when progesterone tonically inhibits prolactin release, serotonin inhibits the release of prolactin. J. Endocr. (1987) 112, 367–374

Role of serotoninergic neurones in the control of gonadotrophin and prolactin secretion in the rat

1982 ◽  
Vol 94 (1) ◽  
pp. 83-89 ◽  
Author(s):  
Csilla Ruzsas ◽  
Patrizia Limonta ◽  
L. Martini
Keyword(s):  
Combined Treatment ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Intact Male ◽  
Prolactin Release ◽  
Lh Secretion ◽  
The Brain

The role of brain serotonin (5-hydroxytryptamine, 5-HT) in the control of LH, FSH and prolactin secretion was studied in two groups of experimental animals: intact adult male rats and ovariectomized adult female rats. 5-Hydroxytryptophan (5-HTP), a precursor of serotonin synthesis, and fluoxetine, a specific inhibitor of 5-HT uptake, were given either alone or together. 5-Hydroxytryptophan (50 mg/kg) was administered intraperitoneally and fluoxetine (20 μg/rat) was given into one of the lateral ventricles of the brain. Neither 5-HTP nor fluoxetine given alone affected LH secretion but combined treatment with the two drugs elicited a significant increase in serum LH levels in both intact male and ovariectomized female rats. Fluoxetine and 5-HTP, alone or together, did not modify FSH secretion in either kind of animal. In intact males and in ovariectomized females, 5-HTP induced a significant increase in prolactin release; fluoxetine alone was ineffective. In male animals treated with fluoxetine plus 5-HTP, serum prolactin levels increased but such an increase was lower than that found in the animals treated only with 5-HTP. In ovariectomized rats, the combined treatment induced an increase in serum prolactin levels similar to that found in animals treated with 5-HTP alone. These data suggested that brain serotonin exerts a stimulating effect on LH secretion in both intact male and ovariectomized rats, but that it does not play any role in the control of FSH release in either kind of animal and that central serotoninergic pathways participate in the stimulating control of prolactin release from the anterior pituitary gland. However, some of the data also suggested the possibility of the existence in the brain of serotoninergic systems inhibiting prolactin secretion.

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

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

Effects of Tamoxifen on Serum Prolactin Levels, Pituitary Immunoreactive Prolactin Cells and Uterine Growth in Estradiol-Treated Ovariectomized Rats

1996 ◽  
Vol 28 (04) ◽  
pp. 171-176 ◽  
Author(s):  
Poli Spritzer ◽  
Maria Ribeiro ◽  
Miriam Oliveira ◽  
Ligia Barbosa-Coutinho ◽  
Ilma Silva ◽  
...  
Keyword(s):  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Prolactin Cells ◽  
Uterine Growth
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