Prolactin Implants in the Hypothalamus Inhibit Prolactin Surges During Pregnancy and Alter Prolactin Release in Response to Dopamine Receptor Blockade

Vidal, Gabriela Pereira; Mathiasen, Joanne R.; Voogt, James L.

doi:10.1111/j.1365-2826.1991.tb00271.x

Cited by 10 publications

(3 citation statements)

References 23 publications

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“…Thus, current evidence suggests that one possible function for prolactin release in the male rat is to modulate central neuronal activity of hypothalamic and extrahypothalamic dopaminergic cells. The increase of dopaminergic activity may also serve as a negative feedback mechanism since dopamine inhibits prolactin release [for review, see 39], A negative feedback role for prolactin is supported by the fact that prolactin implants inhibit prolactin surges during pregnancy [40], Prolactin affects several components of the immune sys tem. Injections of prolactin into rats increase antibody production [41,42], This effect may be mediated by acting on T lymphocytes.…”

Section: Discussionmentioning

confidence: 99%

Ibotenic Acid Lesions in the Bed Nucleus of the Stria terminalis Attenuate Conditioned Stress-Induced Increases in Prolactin, ACTH and Corticosterone

et al. 1993

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The contribution of the bed nucleus of the stria terminalis (BST) to the expression of stress-induced increases in ACTH/corticosterone, prolactin and renin secretion was assessed. Neurons in the lateral part of the BST were destroyed with bilateral injections of the cell-selective neurotoxin ibotenic acid (1.5 µg in 0.1 µl of solution per side). Two weeks later, the rats were stressed using an immobilization or conditioned stress paradigm. Rats with lesions in the lateral part of the BST showed attenuated ACTH and corticosterone responses to conditioned stress. Bilateral ablation of lateral BST significantly reduced the prolactin secretory response to conditioned stress. The same lesions had no effect upon plasma increases in renin that occur in response to conditioned stress. Also, destruction of neurons in the BST did not affect immobilization-induced increases in ACTH, corticosterone, prolactin or renin. Previous studies have demonstrated that ibotenic acid lesions in the central amygdala reduce corticosterone and renin response to conditioned stress. Thus, both the BST and central amygdala are important for the adrenocortical response to conditioned stress. Neurons in the central nucleus of the amygdala are part of the circuitry that mediates renin responses to conditioned stress. Neurons in the BST are important for the full expression of prolactin responses to conditioned stress. The neuronal circuitry and stressor specificity in the mediation of prolactin, renin and ACTH/corticosterone responses are discussed.

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Section: Discussionmentioning

confidence: 99%

Ibotenic Acid Lesions in the Bed Nucleus of the Stria terminalis Attenuate Conditioned Stress-Induced Increases in Prolactin, ACTH and Corticosterone

et al. 1993

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“…Arbogast and Voogt [14] have shown that pituitary PRL content was lower during the nocturnal PRL surge and higher during the diurnal PRL surge. Substantial decreases in pituitary PRL content were also observed during the preovulatory PRL surge [25,30,42,43] and the estradiol-dependent PRL surge [25,44]. It is possible that the lower PRL response to DOM seen during the nocturnal surge was due to less pituitary PRL available for release, and the higher PRL response to DOM during the diurnal surge was due to more PRL available for release.…”

Section: Discussionmentioning

confidence: 99%

Differential Regulation of the Nocturnal and Diurnal Prolactin Surges in Pregnant Rats Revealed by Dopamine Receptor Antagonism

Mathiasen

Voogt²

1992

Neuroendocrinology

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We have explored temporal changes in the magnitude of dopamine (DA) interaction (DA tone) at the anterior pituitary lactotrophs related to both the nocturnal and diurnal prolactin (PRL) surges on day 8 of pregnancy, by utilizing a competitive DA D₂ antagonist, domperidone (DOM). After withdrawal of blood from pregnant rats on day 7 in order to demonstrate the presence of a PRL surge, experimental rats received DOM (100 µg/kg i.v. or i.a.) at various times on day 8. Blood samples were taken immediately before and following injection of DOM at 5, 15, 30 and 60 min. The peak PRL response to DOM occured 15 min after injection. Comparisons were made between circulating PRL levels immediately prior to and at several times following DOM administration for the various times of the day, and represented as incremental increases in PRL following DOM. During times on day 8 when PRL levels were normally low (24:00, 06:00, 12:00 and 16:00 h), pregnant rats exhibited a substantial PRL response to DOM. However, during the nocturnal PRL surge (02:00, 04:00 h) the peak PRL response to DOM was significantly lower. In sharp contrast, the PRL response to DOM administered during the diurnal PRL surge (18:00 h) was significantly higher than all other times of the day tested. In a dose-response study in which 10, 100 and 1,000 µg/kg DOM was administered at the two critical times when the response to DOM differed greatly, 02:00 and 18:00 h, there was a significantly reduced PRL response to DOM at 02:00 h compared to 18:00 h. This suggests that during the nocturnal PRL surge there is a decrease in DA interaction with D₂ receptors on pituitary lactotrophs compared to the diurnal PRL surge in pregnant rats. An alternative explanation is that more PRL-releasing factor is present at 18:00 h, and removal of all the DA inhibitory input to the lactotrophs allows its full expression. In either case, this study provides clear evidence that the two PRL surges during early pregnancy are under different control mechanisms.

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“…Highly developed mammary glands in the cycling rats with Rcho cells indicate the mammotrophic action of the secreted factor. It is possible that PL-I was responsible for the inhibition of PRL synthesis and release, acting like PRL in exerting a negative short-loop feedback on PRL secretion [12,35], although other factors secreted by the Rcho cells could have similar effects. Preliminary experiments from our laboratory show that implantation of recombinant PL-I into the hypothalamus abolishes the nocturnal PRL surge in pregnant rats.…”

Section: Discussionmentioning

confidence: 99%

A Factor(s) from a Rat Trophoblast Cell Line Inhibits Prolactin Secretion in Vitro and in Vivo1

Tomogane

Arbogast

Soares

et al. 1993

Biology of Reproduction

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The purpose of the present study was to measure the inhibitory action of secretions from trophoblast cells on prolactin (PRL) secretion in cycling and pregnant rats, and to determine whether factor(s) from trophoblast cells act directly on anterior pituitary cells. A rat choriocarcinoma cell line (Rcho)--a line consisting of trophoblast cells, including differentiated giant cells that secrete members of the placental PRL family--was used. When Rcho cells (1 x 10(6) cells) were transplanted under the kidney capsule of cycling rats, tumors developed and the rats went into constant diestrus. Eight days after cell injection, plasma progesterone was significantly increased in treated rats compared to controls, whereas plasma and pituitary PRL and pituitary PRL mRNA levels were significantly decreased. Similar PRL results were seen on Day 9 of pregnancy after injection of Rcho cells on Day 0 or Day 1 of pregnancy. To determine whether secretions from Rcho cells had a direct effect on anterior pituitary cells to inhibit PRL release, anterior pituitary cells were enzymatically dispersed and cultured for 4 days. Conditioned medium was obtained from 9-day Rcho cell cultures and concentrated by ultrafiltration. A fraction containing substances with molecular weights greater than 10,000 suppressed PRL release from the pituitary culture after 3 and 24 h. Conditioned medium containing substances with molecular weights between 1000 and 10,000 had no effect on PRL release, nor did conditioned medium from a placental cell line designated HRP-1. HRP-1 also contains trophoblast cells but does not contain the differentiated giant cells.(ABSTRACT TRUNCATED AT 250 WORDS)

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Prolactin Implants in the Hypothalamus Inhibit Prolactin Surges During Pregnancy and Alter Prolactin Release in Response to Dopamine Receptor Blockade

Cited by 10 publications

References 23 publications

Ibotenic Acid Lesions in the Bed Nucleus of the Stria terminalis Attenuate Conditioned Stress-Induced Increases in Prolactin, ACTH and Corticosterone

Ibotenic Acid Lesions in the Bed Nucleus of the Stria terminalis Attenuate Conditioned Stress-Induced Increases in Prolactin, ACTH and Corticosterone

Differential Regulation of the Nocturnal and Diurnal Prolactin Surges in Pregnant Rats Revealed by Dopamine Receptor Antagonism

A Factor(s) from a Rat Trophoblast Cell Line Inhibits Prolactin Secretion in Vitro and in Vivo1

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