Alterations in stress-induced prolactin release in adult female and male rats exposed to stress, in utero

1989 ◽  
Vol 45 (5) ◽  
pp. 1073-1076 ◽  
Author(s):  
Craig Howard Kinsley ◽  
Phyllis E. Mann ◽  
Robert S. Bridges
1994 ◽  
Vol 59 (1) ◽  
pp. 57-62 ◽  
Author(s):  
Graciela S. Díaz-Torga ◽  
Damasia Becú-Villalobos ◽  
Carlos Libertun

1988 ◽  
Vol 2 (13) ◽  
pp. 2874-2877 ◽  
Author(s):  
O. F. X. Almeida ◽  
K. E. Nikolarakis ◽  
G. E. Webley ◽  
A. Herz

1986 ◽  
Vol 108 (3) ◽  
pp. 399-403 ◽  
Author(s):  
R. L. Pérez ◽  
G. A. Machiavelli ◽  
M. I. Romano ◽  
J. A. Burdman

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


1986 ◽  
Vol 5 (4) ◽  
pp. 189-196 ◽  
Author(s):  
R. F. Mankes ◽  
V. Renak ◽  
J. Fieseher ◽  
R. Lefevre

The embryotoxic effects of high doses of the narcotizing ethanol dimer 1,3-butanediol were evaluated in pregnant Long-Evans rats during the “critical period” of organogenesis. Butanediol was given by gavage at levels of 0,7060,4236, or 706 mg/kg per day (24,14.4, or 2.4% of the acute oral LD50 value for rats). Maternal sedation was observed at 7060 and 4236 mg/kg, but feed consumptions and maternal body weights were unaffected. Butanediol caused a significant, dose-dependent decrease in offspring birthweights. At the highest butanediol dose, birthweights were preferentially and significantly decreased in male pups not contiguous in utero to female siblings. Other group I1 offspring were not affected and did not differ significantly from controls. As butanediol was given prior to the period of greatest fetal growth and fetal sex steroidogenests, it is concluded that intra-uterine levels of female sex steroids (estradiol) enhance fetal repair of cellular damage (restitution ad integrum), whereas testosterone inhibits fetal repair or exacerbates previous embryonic damage by some unknown mechanism. Such interaction furthers the concept that intrauterine position affects the endpoints of developmental toxicity, as expressed at partuition.


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 ◽  
...  

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.


Life Sciences ◽  
1991 ◽  
Vol 48 (4) ◽  
pp. 311-320 ◽  
Author(s):  
Agneta Ekman ◽  
Marianne Quiding ◽  
Elias Eriksson

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