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.

scholarly journals Orphanin FQ/Nociceptin Is a Physiological Regulator of Prolactin Secretion in Female Rats

Endocrinology ◽  
2006 ◽  
Vol 147 (11) ◽  
pp. 5087-5093 ◽  
Author(s):  
Matthew Chesterfield ◽  
James Janik ◽  
Emily Murphree ◽  
Courtney Lynn ◽  
Erin Schmidt ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Prolactin Secretion ◽  
Secretory Response ◽  
Female Rats ◽  
Receptor Subtype ◽  
Orphanin Fq ◽  
Prolactin Release ◽  
Endogenous Opioid Peptide ◽  
Male And Female Rats ◽  
Prolactin Response

Orphanin FQ/nociceptin (OFQ/N), the most recently identified endogenous opioid peptide, stimulates prolactin secretion in both male and female rats. OFQ/N, however, did not elicit this stimulatory effect through the μ-, δ-, or κ-opiate receptor subtype. The role OFQ/N plays in prolactin regulation under physiological conditions and its mechanism of action are not known. The purpose of these studies was to determine the physiological significance and pharmacological specificity of the prolactin secretory response to OFQ/N. In addition, the role of the tuberoinfundibular dopaminergic (TIDA) neurons in mediating this response was examined. Opioid receptor-like-1 (ORL-1) receptors were blocked by pretreatment with compound B (Comp B), a purported OFQ/N antagonist, or receptor synthesis was disrupted by pretreatment with ORL-1 receptor antisense oligonucleotides. The prolactin secretory response to OFQ/N administration in diestrous females was measured. Furthermore, the suckling-induced prolactin response was also determined after Comp B pretreatment. TIDA neuronal activity was quantified in diestrous female rats to determine whether OFQ/N stimulates prolactin release by inhibiting TIDA neurons. OFQ/N significantly inhibited the TIDA neurons by 1 min, preceding the prolactin secretory response. Both Comp B and antisense pretreatment blocked the stimulatory effects of OFQ/N on prolactin release, and Comp B abolished the suckling-induced prolactin response. These studies indicate that OFQ/N is a potent stimulus for prolactin secretion in female rats and that it mediates this effect by rapid and transient inhibition of TIDA neuronal activity. Furthermore, OFQ/N plays a physiologically significant role in the regulation of prolactin secretion during lactation, and it mediates its effects via actions at the ORL-1 receptor subtype.

Feedback regulation by progesterone of stress-induced prolactin release in rats

1989 ◽  
Vol 120 (1) ◽  
pp. 37-43 ◽  
Author(s):  
R. P. Deis ◽  
E. Leguizamon ◽  
G. A. Jahn
Keyword(s):  
Prolactin Secretion ◽  
Female Rats ◽  
Male Rats ◽  
Serum Prolactin ◽  
Progesterone Concentration ◽  
Prolactin Release ◽  
Serum Progesterone ◽  
Progesterone Secretion ◽  
Male And Female Rats

ABSTRACT We have previously found that modifications to serum progesterone concentration have profound inhibitory effects on prolactin release in response to ether stress. The objective of the present study was to determine the effect of ether stress on progesterone secretion and the role of this steroid in ether-induced prolactin release. Serum progesterone concentration, 5 min after ether stress had been applied over a 2-min period, was consistently increased in male rats, in cyclic rats on the mornings of pro-oestrus and oestrus, and in androgenized rats in permanent oestrus. Ovariectomized androgenized rats showed the same response. Adrenalectomy of male and female rats abolished the progesterone increase induced by stress. Thus, the progesterone secreted by stressed rats is mostly of adrenal origin. In groups of male and pro-oestrous rats, circulating concentrations of prolactin and progesterone were measured from 5 to 60 min after stress. In both sexes the serum prolactin concentration was significantly increased at only 5 and 10 min after stress when compared with control values. In pro-oestrous rats the serum progesterone concentration was significantly higher than in controls at 5, 10 and 20 min after stress, whilst in male rats the concentration remained significantly higher at 30 min. Thirty minutes after the first stress, male and pro-oestrous rats were etherized for 2 min, and bled 5 min after removal from the ether container. In female rats this second stress produced only a slight but significant increase in serum prolactin concentrations, whereas in male rats prolactin concentrations did not increase. The second stress was still capable of significantly increasing circulating progesterone concentrations to levels similar to those obtained after the first stress in animals from all groups. Thus, an increased circulating progesterone concentration did not lead to regulation of further progesterone secretion. To find whether this type of response was due to a blocking effect of the previously released progesterone, animals were injected with the anti-progesterone RU 38486 (17β-hydroxy-11β-(4-dimethylaminophenyl)-17α-propinyl-oestra-4,9-dien-3-one) or with a specific antibody raised against progesterone. In both groups of treated rats the second stress induced a significant increase in serum prolactin and progesterone concentrations to give values similar to those obtained after the first stress. When the second stress was applied to female rats 60 min after the first the prolactin response was comparable to that obtained after the first exposure to ether. In conclusion, we have demonstrated that serum prolactin and progesterone concentrations are significantly increased after ether stress, and that the latter hormone exerts an inhibitory regulatory feedback on prolactin secretion. These results provide an important new insight into the role of progesterone in the regulation of prolactin release. Journal of Endocrinology (1989) 120, 37–43

SENSITIVITY OF ANTERIOR HYPOTHALAMIC AREAS TO GONADAL STEROID IMPLANTATION IN ANDROGENIZED FEMALE RATS

1977 ◽  
Vol 74 (2) ◽  
pp. 315-NP ◽  
Author(s):  
A. DANGUY ◽  
J. L. PASTEELS ◽  
F. ECTORS
Keyword(s):  
Single Injection ◽  
Mammary Glands ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Male Rats ◽  
Control Synthesis ◽  
Normal Female ◽  
Immunofluorescence Studies ◽  
Oestradiol Benzoate ◽  
Stimulation Of

A single injection of 1 mg of a complex of testosterone esters on day 5 of life was used to prepare constantly oestrous rats. Such androgenized female rats were then ovariectomized and submitted to stereotaxical implantation of 1 μg oestradiol benzoate, 5 μg testosterone isobutyrate or, as a control, 10 μg cholesterol in the anterior hypothalamic areas. The effects of the steroids on plasma and pituitary FSH and LH were assessed by radioimmunoassay. As reported previously by us in normal female and male rats, the preoptic–suprachiasmatic area (POA) was able to control synthesis and secretion of both gonadotrophins and did not lose its sensitivity to oestradiol and testosterone in androgenized rats. Evidence for enhanced prolactin secretion in androgenized rats was derived from immunofluorescence studies of the pituitary gland and from histology of the mammary glands. In this respect the condition of the androgenized females was opposite to that of the males. The present work demonstrated that stimulation of prolactin secretion in androgenized female rats resulted from oestrogen action due to permanent oestrus rather than from impairment of hypothalamo-hypophysial relationships. Indeed, prolactin stimulation was suppressed when the androgenized rats were ovariectomized and restored when they were subsequently implanted with oestradiol in the POA.

INDUCTION OF PROLACTIN AND LUTEINIZING HORMONE RELEASE BY HISTAMINE IN MALE AND FEMALE RATS AND THE INFLUENCE OF BRAIN TRANSMITTER ANTAGONISTS

1978 ◽  
Vol 76 (2) ◽  
pp. 193-202 ◽  
Author(s):  
A. O. DONOSO
Keyword(s):  
Prolactin Secretion ◽  
Oestrous Cycle ◽  
Female Rats ◽  
Male Rats ◽  
Intraventricular Injection ◽  
Hormone Release ◽  
Stimulatory Action ◽  
Male And Female Rats ◽  
Oestradiol Benzoate ◽  
Lh Release

The levels of prolactin and LH in the plasma of rats were determined at various times after intraventricular injection of histamine. Doses of 5 and 60 μg histamine (free base) in male rats, anaesthetized with ether, induced an increase in the level of prolactin in the plasma, whilst producing a slight decrease in the concentration of LH. Injection of 5 μg histamine at 14.00 h into female rats at all stages of the oestrous cycle caused prolactin to be released; the effect was greatest at oestrus and at day 1 of dioestrus. Histamine also gave rise to a marked increase in the level of LH in the plasma when administered to pro-oestrous rats, but had no effect when injected at the other stages of the oestrous cycle. The effect of histamine on the release of prolactin in ovariectomized, oestradiol benzoate: progesterone-primed (OVX,OB:P) rats was found to be dose-related, and the level of LH in the plasma was increased by as little as 1·25 μg. Pretreatment with adrenergic (phenoxybenzamine and propranolol) and cholinergic (atropine) antagonists failed to block the stimulatory effects of histamine on prolactin secretion, but pretreatment with methysergide (serotonin antagonist) increased the histamine-induced release of prolactin in male rats. Antagonists did not modify the response of prolactin to histamine in OVX,OB:P-primed rats. The histamine-induced release of LH in OVX,OB:P-primed rats was slightly reduced by pretreatment with phenoxybenzamine, propranolol and atropine, but not by methysergide. These results indicate that histamine facilitates the release of prolactin. The stimulatory action of histamine on both pro-oestrous and OVX,OB:P-primed but not male rats suggests that histamine may be involved in LH release in the rat. Results obtained in animals pretreated with transmitter antagonists, which were unable to prevent histamine-induced hormone release, suggest that the actions of this amine are not mediated by cholinergic, noradrenergic or serotonergic mechanisms.

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.

THE EFFECT OF 2-BROMO-α-ERGOCRYPTINE AND 2-CHLORO-α-METHYLERGOLINE-8β-ACETONITRILE (LERGOTRILE MESYLATE) ON THE PROLACTIN SECRETION OF THE EWE

1977 ◽  
Vol 86 (4) ◽  
pp. 722-727 ◽  
Author(s):  
R. D. Hooley ◽  
L. R. Fell ◽  
J. K. Findlay
Keyword(s):  
Luteal Phase ◽  
Ergot Alkaloids ◽  
Prolactin Secretion ◽  
Oestrous Cycle ◽  
Basal Secretion ◽  
Prolactin Release ◽  
Methane Sulphonate ◽  
Prolactin Response

ABSTRACT The effects of two ergot alkaloids, 2-bromo-α-ergocryptine methane-sulphonate (CB154, Sandoz) and lergotrile mesylate (LM, E. Lilly & Co.), on the basal secretion of prolactin and on the prolactin response to TRH or the milking stimulus was investigated in the sheep. Both CB154 (c. 0.5 mg/kg) and LM (c. 0.75 mg/kg) markedly reduced basal levels of prolactin and inhibited the TRH-induced prolactin release in ewes in the mid-luteal phase of the oestrous cycle. Both compounds also suppressed basal levels of prolactin in lactating ewes and inhibited the prolactin response to the milking stimulus in lactating ewes.

THE EFFECTS OF THE DOPAMINE AGONIST, LERGOTRILE MESYLATE, ON PROLACTIN SECRETION IN WOMEN

1978 ◽  
Vol 87 (1) ◽  
pp. 12-18 ◽  
Author(s):  
Wayne Leebaw ◽  
Louyse Lee ◽  
Paul Woolf
Keyword(s):  
Growth Hormone ◽  
Dopamine Agonist ◽  
Prolactin Secretion ◽  
Entire Group ◽  
Prolactin Release ◽  
Chronic Therapy ◽  
The Mean ◽  
Prolactin Response ◽  
Nocturnal Rise ◽  
Ergot Derivative

ABSTRACT Lergotrile mesylate, an ergot derivative and dopamine agonist, decreases basal (single sample) prolactin levels and blunts phenothiazine-mediated prolactin release. To more thoroughly evaluate the effect of this drug, we measured prolactin and growth hormone concentrations hourly over 24 h in 5 healthy women and during insulin (0.1 U/kg) induced hypoglycaemia (ITT) in 6 women before and during 2-day lergotrile treatment. Lergotrile (4.0 to 6.0 mg/day) significantly decreased the mean 24-hour prolactin concentration in 3 and abolished the nocturnal rise in 4. For the entire group, the mean nocturnal levels (2400–0700 hours) were 24.0 #x00B1;7.5 vs 14.4 ± 3.9 ng/ml during waking (0800–2300 hours) pre-lergotrile (P<0.05), while during therapy the concentrations were 8.9 ± 2.8 vs 8.0 ± 1.4 ng/ml (NS), respectively. The prolactin response to ITT was also significantly inhibited by lergotrile with the peak response reduced from 78.2 ± 35.1 ng/ml to 9.0 ± 3.6 ng/ml (P < 0.05). The mean 24-hour growth hormone concentration was unchanged during therapy, and there was no significant effect on the GH response during ITT. The effects of chronic therapy with lergotrile (8 mg/day for 6 weeks) were studied in one acromegalic patient with elevated levels of prolactin and growth hormone. Her prolactin concentration fell from 452.2 ± 8.0 to 216 ng/ml, while GH declined from 23.8 ± 1.3 to 14.8 ng/ml. Lergotrile mesylate effectively lowers mean 24-hour prolactin concentrations (determined hourly) and completely abolishes both nocturnal and hypoglycaemia-mediated prolactin release. This drug may also be beneficial in the therapy of acromegaly.

ROLE OF OESTROGENS AND GONADOTROPHINS IN PERPHENAZINE-INDUCED MAMMOGENESIS

1970 ◽  
Vol 48 (3) ◽  
pp. 365-371 ◽  
Author(s):  
A. DANON ◽  
C. P. WELLER ◽  
F. G. SULMAN
Keyword(s):  
Median Eminence ◽  
Mammary Glands ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Gonadotrophin Secretion

SUMMARY Treatment of intact or recently (1 day) ovariectomized female rats with 5 mg perphenazine (Trilafon)/kg/day for 5 days resulted in marked lobulo—alveolar differentiation of the mammary glands. Perphenazine failed to stimulate mammogenesis in chronically (12 days) ovariectomized rats, unless they had been primed with oestradiol. However, mammogenic effects in chronically ovariectomized rats were obtained after implantation of minute amounts (2 μg) of oestradiol into the median eminence, or after treatment for 16 days with the non-steroid pituitary gonadotrophin-inhibitor methallibure (ICI 33828; 20 mg/kg/day). Since these latter procedures counteract the gonadotrophin surge after ovariectomy, it would appear that inhibition of gonadotrophin secretion is necessary before prolactin secretion can be stimulated by perphenazine. Castrated male rats responded to perphenazine with lobulo—alveolar differentiation similar to that in intact males. The implications of this difference with regard to the mechanism of pituitary response to gonadectomy are discussed.

scholarly journals Effect of blockade of postsynaptic H1 or H2 receptors or activation of presynaptic H3 receptors on catecholamine-induced stimulation of ACTH and prolactin secretion

2000 ◽  
pp. 637-641 ◽  
Author(s):  
E Willems ◽  
U Knigge ◽  
H Jorgensen ◽  
A Kjaer ◽  
J Warberg
Keyword(s):  
Receptor Antagonist ◽  
Prolactin Secretion ◽  
Male Rats ◽  
H2 Receptor Antagonist ◽  
Histaminergic System ◽  
Intracerebroventricular Infusion ◽  
H2 Receptors ◽  
H3 Receptors ◽  
Prolactin Response ◽  
Stimulation Of

The effect of inhibition of the neuronal histaminergic system by blockade of postsynaptic H1 or H2 receptors or activation of presynaptic H3 autoreceptors on the ACTH and prolactin responses to the catecholamines epinephrine and norepinephrine was investigated in conscious male rats. Intracerebroventricular infusion of epinephrine and norepinephrine stimulated ACTH and prolactin secretion. Prior intracerebroventricular infusion of the H1 receptor antagonist, mepyramine, or the H2 receptor antagonist, cimetidine, had no effect on the ACTH response to epinephrine or norepinephrine, while these responses were inhibited by pretreatment with the H3 receptor agonist, imetit. The prolactin response to norepinephrine was significantly inhibited by pretreatment with mepyramine, cimetidine or imetit whereas the three histaminergic compounds had no effect on the prolactin response to epinephrine. The findings suggest that the histaminergic system exerts a mediating or permissive action on the norepinephrine-induced stimulation of prolactin secretion, whereas an intact histaminergic system may not be required for catecholamines to stimulate ACTH secretion. The inhibitory effect of imetit on catecholamine-induced release of ACTH may be due to an activation of H3 receptors located presynaptically on non-histaminergic neurons, e.g. aminergic neurons. The study further indicates an important role of histamine in the neuroendocrine regulation of prolactin secretion.

RELATIONSHIP BETWEEN THE PITUITARY GLAND AND GONADAL STEROIDS: INVOLVEMENT OF A HYPOPHYSIAL FACTOR IN REDUCED α2u-GLOBULIN AND INCREASED TRANSCORTIN CONCENTRATIONS IN RAT SERUM

1978 ◽  
Vol 78 (1) ◽  
pp. 31-38 ◽  
Author(s):  
G. VANDOREN ◽  
H. VAN BAELEN ◽  
G. VERHOEVEN ◽  
P. DE MOOR
Keyword(s):  
Pituitary Gland ◽  
Testosterone Propionate ◽  
Single Injection ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Male Rats ◽  
Rat Serum ◽  
Mediated Effects ◽  
Male And Female Rats ◽  
Oestradiol Benzoate

Evidence is presented that the level of α2u-globulin in the serum of male rats depends, at least in part, on neonatal androgens. After castration of adult animals the concentration of this protein falls but remains measurable, whereas in intact or ovariectomized female rats α2u-globulin cannot be detected. Moreover, α2u-globulin is found in adult male and female rats gonadectomized at birth and treated with a single injection of testosterone propionate immediately thereafter. The mechanism by which neonatal androgens increase the concentration of α2u-globulin has been investigated. Transplantation of a supplementary pituitary gland under the renal capsule of male rats resulted in reduced levels of α2u-globulin and increased levels of transcortin. The changes discussed here were observed only in those animals in which the transplant was functional and they were amplified or reversed by modulators of prolactin secretion such as oestrogens or bromocriptine respectively. The hypothesis is advanced that neonatal androgens stimulate the production of a hypothalamic inhibitory factor that controls the secretion of prolactin, or another hypophysial hormone subjected to similar neuroendocrine control. Measurements in gonadectomized animals and in rats receiving both oestradiol benzoate and bromocriptine indicate that, besides these pituitary-mediated effects, both oestrogens and androgens exert direct effects on the level of α2u-globulin.

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