CORRELATION BETWEEN THE EFFECTS OF NEUROLEPTICS ON PROLACTIN RELEASE, MAMMARY STIMULATION AND THE VAGINAL CYCLE IN RATS

1978 ◽  
Vol 76 (3) ◽  
pp. 507-515 ◽  
Author(s):  
W. LOTZ ◽  
R. KRAUSE
Keyword(s):  
Mammary Gland ◽  
Dose Dependence ◽  
Clinical Syndrome ◽  
Female Rats ◽  
Male Rats ◽  
Test Model ◽  
Neuroleptic Drugs ◽  
Prolactin Release ◽  
Luteinizing Hormone Releasing Hormone ◽  
Daily Oral Administration

The correlation between hyperprolactinaemia induced by the administration of neuroleptic drugs, disturbances of the vaginal cycle and mammary gland stimulation in rats was investigated as a test model simulating the clinical syndrome of hyperprolactinaemia and amenorrhoea with anovulation. In acute experiments in which clozapine, sulpiride and chlorpromazine were administered orally to rats of both sexes, there were rapid increases in the level of prolactin in the serum with peak values between 15 and 60 min. The responses of female rats to various doses of sulpiride were consistently higher than those of male rats. Hyperprolactinaemia induced by sulpiride in dioestrous rats failed to desensitize the ovaries to the ovulatory effect of exogenous luteinizing hormone releasing hormone. Studies of these substances and of metoclopramide, haloperidol and thioridazine were then carried out in female rats by daily oral administration over a period of 13 days. The increases in the level of prolactin in the serum were paralleled by disruption of the vaginal cycle up to and including constant dioestrus and by mammary gland stimulation which, like the preceding phenomena, showed dose-dependence. The potencies of these six neuroleptics, as estimated from their effects on the mammary gland, appeared to be haloperidol⪢ sulpiride ≥ metoclopramide = thioridazine > chlorpromazine > clozapine.

scholarly journals Kisspeptin Stimulation of Prolactin Secretion Requires Kiss1 Receptor but Not in Tuberoinfundibular Dopaminergic Neurons

Endocrinology ◽  
2019 ◽  
Vol 160 (3) ◽  
pp. 522-533 ◽  
Author(s):  
Nayara S S Aquino ◽  
Ilona C Kokay ◽  
Carolina Thörn Perez ◽  
Sharon R Ladyman ◽  
Patricia C Henriques ◽  
...  
Keyword(s):  
Dopaminergic Neurons ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Male Rats ◽  
Prolactin Release ◽  
Whole Cell Patch Clamp ◽  
Neuropeptide Ff ◽  
Concomitant Reduction ◽  
Prolactin Response

Abstract Kisspeptin has been shown to stimulate prolactin secretion. We investigated whether kisspeptin acts through the Kiss1 receptor (Kiss1r) to regulate dopamine and prolactin. Initially, we evaluated prolactin response in a Kiss1r-deficient mouse line, in which Kiss1r had been knocked into GnRH neurons (Kiss1r−/−R). Intracerebroventricular kisspeptin-10 (Kp-10) increased prolactin release in wild-type but not in Kiss1r−/−R female mice. In ovariectomized, estradiol-treated rats, the Kiss1r antagonist kisspeptin-234 abolished the Kp-10–induced increase in prolactin release but failed to prevent the concomitant reduction in the activity of tuberoinfundibular dopaminergic (TIDA) neurons, as determined by the 3,4-dihydroxyphenylacetic acid/dopamine ratio in the median eminence. Using whole-cell patch clamp recordings in juvenile male rats, we found no direct effect of Kp-10 on the electrical activity of TIDA neurons. In addition, dual-label in situ hybridization in the hypothalamus of female rats showed that Kiss1r is expressed in the periventricular nucleus of the hypothalamus (Pe) and arcuate nucleus of the hypothalamus (ARC) but not in tyrosine hydroxylase (Th)–expressing neurons. Kisspeptin also has affinity for the neuropeptide FF receptor 1 (Npffr1), which was expressed in the majority of Pe dopaminergic neurons but only in a low proportion of TIDA neurons in the ARC. Our findings demonstrate that Kiss1r is necessary to the effect of kisspeptin on prolactin secretion, although TIDA neurons lack Kiss1r and are electrically unresponsive to kisspeptin. Thus, kisspeptin is likely to stimulate prolactin secretion via Kiss1r in nondopaminergic neurons, whereas the colocalization of Npffr1 and Th suggests that Pe dopaminergic neurons may play a role in the kisspeptin-induced inhibition of dopamine release.

Involvement of cGMP in LHRH-stimulated gonadotropin release.

1978 ◽  
Vol 235 (6) ◽  
pp. E586 ◽  
Author(s):  
Z Naor ◽  
C P Fawcett ◽  
S M McCann
Keyword(s):  
Mechanism Of Action ◽  
Female Rats ◽  
Male Rats ◽  
Camp Content ◽  
Luteinizing Hormone Releasing Hormone ◽  
Gonadotropin Release ◽  
Male And Female Rats ◽  
The Relationship ◽  
Stimulation Of

Anterior pituitary content of cyclic AMP (cAMP) and cyclic GMP (cGMP) has been measured during stimulation of gonadotropin release by luteinizing-hormone-releasing hormone (LHRH) in vitro to gain more information concerning the relationship between the mechanism of action of LHRH and cyclic nucleotides. During the increased gonadotropin release obtained by incubation by hemipituitaries with LHRH (0.25--25 X 10(-9) M) for 180 min, the glands taken from both male and female rats exhibited increased cGMP content, whereas cAMP content rose only in those taken from male rats. The increase in cGMP content was observed after only 2 min in the presence of LHRH (5 X 10(-9) M) and prior to augmented gonadotropin release. The increase in cAMP content in the male glands was detectable only after 60 min of incubation. These results suggest that cGMP might be involved in the mechanism of action of LHRH.

PROLACTIN STIMULATION TEST WITH PERPHENAZINE: AN EVALUATION OF PLASMA PROLACTIN LEVELS AND PITUITARY SECRETORY ACTIVITY IN THE RAT

1976 ◽  
Vol 68 (3) ◽  
pp. 355-368 ◽  
Author(s):  
A. A. VAN DER GUGTEN ◽  
P. C. SAHULEKA ◽  
G. H. VAN GALEN ◽  
H. G. KWA
Keyword(s):  
Adult Male ◽  
Secretory Activity ◽  
Female Rats ◽  
Male Rats ◽  
Plasma Prolactin ◽  
Prolactin Release ◽  
Oestrogen Treatment ◽  
Endocrine Status ◽  
Pituitary Prolactin ◽  
Single Plasma

SUMMARY Many investigations of the regulation of prolactin synthesis and release are based on single plasma prolactin determinations. The purpose of the present experiment was to ascertain whether groups of rats (i.e. young or adult, male or female animals, being either intact, gonadectomized or gonadectomized and treated with oestrone), differing in age and/or endocrine status, will react to a single dose of perphenazine by an acute release of pituitary prolactin in proportion to their initial plasma prolactin levels. No consistent relation existed between the classification of the twelve groups of rats into three categories of basal plasma prolactin levels (i.e. < 20, 25–50, > 125 ng/ml) and their response to perphenazine. Even though all groups showed a highly significant increase of plasma prolactin levels the magnitude of the maximum prolactin response at 30 min varied greatly within the groups of one category and thus was not related to the initial prolactin levels. The effect of 14 days of oestrone treatment in increasing plasma prolactin levels in gonadectomized animals was greatest in young and adult male rats, less in young females and not significant in adult females. The results obtained after perphenazine treatment in the latter group made it clear that the effect of oestrogen treatment on prolactin release can be completely blocked by increasing synthesis and/or release of the prolactin-release inhibiting factor (PIF). Since perphenazine induces decrease of pituitary prolactin and a concomitant increase of plasma prolactin levels through lowered PIF-action, the positive effect of oestrogens on prolactin release (as observed in gonadectomized male and young female rats) apparently is caused by a different mode of action. The implications of these findings for the regulation of prolactin release, as affected by the endocrine status of the rat, is discussed. Moreover, comparison of prolactin lost from the pituitary and gained in the circulation of the experimental animals, with amounts of prolactin that were observed to disappear from plasma during the experiment, provided suggestive evidence that the capacity to synthesize and/or eliminate prolactin, after a sudden provoked release of the hormone, differed among the groups. The rates of synthesis by the pituitary, of release from the pituitary into the circulation as well as of elimination of the hormone from the circulation (equally involved in determining actual plasma levels) are thought, therefore, to be far more important for the elucidation of prolactin regulation than single plasma prolactin determinations.

OXYGEN UPTAKE OF RAT MAMMARY TISSUE SLICES

1950 ◽  
Vol 28e (5) ◽  
pp. 217-221 ◽  
Author(s):  
Jules Tuba ◽  
Herbert E. Rawlinson ◽  
Lorna Glen Shaw
Keyword(s):  
Mammary Gland ◽  
Oxygen Uptake ◽  
In Vitro Study ◽  
Female Rats ◽  
Male Rats ◽  
Mammary Tissue ◽  
Oxygen Utilization ◽  
Tissue Slices ◽  
Mammary Gland Tissue

An in vitro study has been made of the oxygen uptake of mammary gland tissue of female rats in various experimental states. Because of the very high proportion of fat in mammary tissue the values of [Formula: see text] are determined on a fat-free as well as a water-free basis, thus providing a more accurate measure of the oxygen consumption of this tissue. The oxygen utilization by mammary gland of pregnant animals is increased approximately three times over the activity in the normal, or resting, gland. This increase is maintained during lactation and a return toward normal levels occurs during postlactational involution. The response to p-phenylenediamine indicated that during lactation the increased energy requirements decreased the reserves of the cytochrome system in mammary tissue. There is a well developed mammary gland in adult male rats; but the average fat content and response to p-phenylenediamine of the tissue are almost identical with values for adult female rats. The use of p-phenylenediamine as a histological stain for the cytochrome system in mammary tissue is described.

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.

Effects of aging on prolactin release after stress in female and male rats

1984 ◽  
Vol 107 (3) ◽  
pp. 337-339 ◽  
Author(s):  
Ljiljana Milenković ◽  
Ljubica Bogić ◽  
Biljana Mušicki ◽  
Jovo V. Martinović
Keyword(s):  
Acute Stress ◽  
Female Rats ◽  
Male Rats ◽  
Elderly Male ◽  
Prolactin Release ◽  
Response To Stress ◽  
Reverse Relationship ◽  
Effects Of Aging ◽  
Sexually Mature ◽  
Intact Rats

Abstract. Young adult and elderly male and female intact rats, as well as chronically ovariectomized (OVX) young and elderly female rats, were subjected to an acute stress by cutting the tip of the tail and prolactin (Prl) concentrations were measured in their blood collected by decapitation at various times thereafter. Maximum concentrations of the hormone were markedly lower in all the three groups of elderly rats than those found in the corresponding young animals, and appeared to occur with a delay in the females, but not in the males. In addition, the Prl-response to stress was attenuated in OVX animals regardless of their age. The result of these experiments, performed at two points on the age scale, suggests that in sexually mature rats of both sexes the stress-induced secretion of Prl is inversely related to the age of the animal and that the reverse relationship is retained in OVX females.

Sex difference in LH response to LHRH and DBcAMP and effect of testosterone.

1978 ◽  
Vol 235 (3) ◽  
pp. E291
Author(s):  
L K Tang
Keyword(s):  
Luteinizing Hormone ◽  
Sex Difference ◽  
Female Rats ◽  
Male Rats ◽  
Camp Production ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Release

Because luteinizing hormone-releasing hormone (LHRH) stimulates both pituitary cAMP production and LH release, cAMP has been implicated in the action of LHRH on LH release. The effects of LHRH and DBcAMP on LH release were tested in 4-h incubations with pituitary cultures prepared from male or female rats. LH contents in medium and cells were separately determined by radioimmunoassays. LH release in response to 10 nM LHRH was significantly greater in cultures prepared from female rats (female-RPC) than in cultures prepared from male rats (male-RPC), 1,070 and 418% of control, respectively. Addition of DBcAMP (3, 5, or 10 mM) significantly stimulated LH release by female-RPC (212, 206, or 286% of control, respectively) but did not affect LH release in male-RPC. Furthermore, DBcAMP significantly increased the cellular LH content in female- but not in male-RPC. Testosterone pretreatment of female-RPC significantly lowered the LHRH-induced LH release but did not affect the DBcAMP-induced LH release. These data indicate that testosterone may contribute to the sex difference in pituitary LH response to LHRH but not to DBcAMP.

EFFECT OF ANDROGENISATION ON ADENOHYPOPHYSIAL PROLACTIN CONTENT IN RATS

1967 ◽  
Vol 54 (4) ◽  
pp. 663-667 ◽  
Author(s):  
M. Kurcz ◽  
K. Kovács ◽  
T. Tiboldi ◽  
A. Orosz
Keyword(s):  
Mammary Gland ◽  
Postnatal Period ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Early Postnatal Period ◽  
Male Rats ◽  
Hormone Production ◽  
Prolactin Content

ABSTRACT The adenohypophyses of androgenised female rats contain significantly less prolactin than control animals. Testosterone phenylpropionate administered in the early postnatal period does not markedly change the adenohypophysial prolactin content of male rats. Since examination of the mammary gland provide no evidence of increased prolactin secretion, the decrease in the adenohypophysial prolactin content of androgenised female rats must be explained by reduced hormone production. It is suggested that androgenisation in female rats influences prolactin production by an action on the hypothalamus.

Effects of LHRH and ANG II on prolactin stimulation are mediated by hypophysial AT1 receptor subtype

1994 ◽  
Vol 266 (2) ◽  
pp. E274-E278 ◽  
Author(s):  
D. Becu-Villalobos ◽  
I. M. Lacau-Mengido ◽  
S. M. Thyssen ◽  
G. S. Diaz-Torga ◽  
C. Libertun
Keyword(s):  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Female Rats ◽  
Receptor Subtype ◽  
Receptor Subtypes ◽  
Ang Ii ◽  
Prolactin Release ◽  
Luteinizing Hormone Releasing Hormone ◽  
Prolactin Response

We have used the nonpeptide angiotensin II (ANG II) receptor antagonists losartan (receptor subtype AT1) and PD-123319 (AT2) to determine the participation of ANG II receptor subtypes in luteinizing hormone-releasing hormone (LHRH)-induced prolactin release in a perifusion study using intact pituitaries in vitro. LHRH (1.85 x 10(-7) M) released prolactin consistently, whereas losartan (10(-5) M) abolished prolactin response without modifying basal prolactin or luteinizing hormone (LH) and follicle-stimulating hormone (FSH) release. PD-123319 (10(-5) M) had no effect on basal or LHRH-induced prolactin, LH, or FSH release. We also determined that the effect of ANG II on prolactin release was mediated by the same receptor subtype. In adenohypophysial cells dispersed in vitro ANG II (10(-8) M) released prolactin. Losartan (10(-7) and 10(-6) M), but not PD-123319, inhibited this effect. We conclude that in intact hypophyses of 15-day-old female rats the effect of LHRH on prolactin release is readily demonstrated. LHRH-induced prolactin release appears to be mediated by ANG II acting in a paracrine manner on AT1 receptors located on lactotrophs.

scholarly journals Physiological and Biochemical Markers of the Sex-Specific Sensitivity to Epileptogenic Factors, Delayed Consequences of Seizures and Their Response to Vitamins B1 and B6 in a Rat Model

2021 ◽  
Vol 14 (8) ◽  
pp. 737
Author(s):  
Vasily A. Aleshin ◽  
Anastasia V. Graf ◽  
Artem V. Artiukhov ◽  
Alexandra I. Boyko ◽  
Alexander L. Ksenofontov ◽  
...  
Keyword(s):  
Sex Differences ◽  
Therapeutic Potential ◽  
Dose Dependence ◽  
Female Rats ◽  
Male Rats ◽  
Long Term Effects ◽  
Pyridoxal Kinase ◽  
Delayed Effects ◽  
The Brain ◽  
Physiological And Biochemical

The disturbed metabolism of vitamins B1 or B6, which are essential for neurotransmitters homeostasis, may cause seizures. Our study aims at revealing therapeutic potential of vitamins B1 and B6 by estimating the short- and long-term effects of their combined administration with the seizure inductor pentylenetetrazole (PTZ). The PTZ dose dependence of a seizure and its parameters according to modified Racine’s scale, along with delayed physiological and biochemical consequences the next day after the seizure are assessed regarding sexual dimorphism in epilepsy. PTZ sensitivity is stronger in the female than the male rats. The next day after a seizure, sex differences in behavior and brain biochemistry arise. The induced sex differences in anxiety and locomotor activity correspond to the disappearance of sex differences in the brain aspartate and alanine, with appearance of those in glutamate and glutamine. PTZ decreases the brain malate dehydrogenase activity and urea in the males and the phenylalanine in the females. The administration of vitamins B1 and B6 24 h before PTZ delays a seizure in female rats only. This desensitization is not observed at short intervals (0.5–2 h) between the administration of the vitamins and PTZ. With the increasing interval, the pyridoxal kinase (PLK) activity in the female brain decreases, suggesting that the PLK downregulation by vitamins contributes to the desensitization. The delayed effects of vitamins and/or PTZ are mostly sex-specific and interacting. Our findings on the sex differences in sensitivity to epileptogenic factors, action of vitamins B1/B6 and associated biochemical events have medical implications.

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