scholarly journals Tyrosine Hydroxylase and Dopamine Transporter Expression in Lactotrophs from Postlactating Rats: Involvement in Dopamine-Induced Apoptosis

Endocrinology ◽  
2007 ◽  
Vol 148 (6) ◽  
pp. 2698-2707 ◽  
Author(s):  
Arnaud Jaubert ◽  
Guillaume Drutel ◽  
Thierry Leste-Lasserre ◽  
François Ichas ◽  
Laurence Bresson-Bepoldin
Keyword(s):  
Tyrosine Hydroxylase ◽  
Pituitary Gland ◽  
Caspase 3 ◽  
D2 Receptor ◽  
Prolactin Secretion ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
Mitochondrial Membrane Potential Loss ◽  
Induced Apoptosis ◽  
Transporter Expression

Cessation of lactation causes a massive loss of surplus lactotrophs in the rat pituitary gland. The factors and mechanisms involved in this phenomenon have not yet been elucidated. Besides its inhibitory control on prolactin secretion and lactotroph proliferation, evidence suggests that dopamine (DA) may be a proapoptotic factor for lactotrophs. We therefore tested the proapoptotic effect of DA on pituitary glands from virgin, lactating, and postlactating rats. By measuring mitochondrial membrane potential loss, caspase-3 activation, and nuclear fragmentation, we show that DA induces apoptosis specifically in lactotrophs from postlactating rats. We then determined that this effect was partly mediated by the DA transporter (DAT) rather than the D2 receptor, as corroborated by the detection of DAT expression exclusively in lactotrophs from postlactating rats. We also observed tyrosine hydroxylase (TH) expression in postlactating lactotrophs that was accompanied by an increase in DA content in the anterior pituitary gland of postlactating compared with virgin rats. Finally, we observed that cells expressing TH coexpressed DAT and cleaved caspase-3. These findings show that DA may play a role in lactotroph regression during the postlactation period by inducing apoptosis. The fact that this process requires DAT and TH expression by lactotrophs themselves suggests that it may be “autocrine” in nature.

Co-localization of tyrosine hydroxylase (TH)- and serotonin (5-HT)-immunoreactive innervation in the rat pituitary gland

1988 ◽  
Vol 94 (1-2) ◽  
pp. 39-45 ◽  
Author(s):  
L.C. Saland ◽  
J.A. Wallace ◽  
A. Samora ◽  
L. Gutierrez
Keyword(s):  
Tyrosine Hydroxylase ◽  
Pituitary Gland ◽  
Rat Pituitary

2-HYDROXYOESTRADIOL INHIBITS PROLACTIN RELEASE FROM THE SUPERFUSED RAT PITUITARY GLAND

1981 ◽  
Vol 90 (3) ◽  
pp. 315-322 ◽  
Author(s):  
ELIZABETH A. LINTON ◽  
NICKI WHITE ◽  
OFELIA LIRA DE TINEO ◽  
S. L. JEFFCOATE
Keyword(s):  
Pituitary Gland ◽  
Prolactin Secretion ◽  
Male Rat ◽  
Prolactin Release ◽  
Rat Pituitary ◽  
Lh Release

The effects of 2-hydroxyoestradiol (2OH-OE2), dopamine, oestradiol-17β and 2OH-OE2 plus dopamine on prolactin and LH release from the male rat pituitary gland were examined in vitro. 2-Hydroxyoestradiol reduced prolactin secretion by 51% at 10−10 mol/l and by 34% at 10−7 mol/l, while oestradiol-17β had no effect at these doses. Dopamine alone (5 × 10−7 mol/l) decreased prolactin released by 58%, 2OH-OE2 plus dopamine produced a similar inhibition of 60%. No significant effect on LH release was observed throughout.

EFFECT OF TESTOSTERONE PROPIONATE ON THE RELEASE OF FSH FROM THE PITUITARY GLAND

1968 ◽  
Vol 57 (2) ◽  
pp. 289-295 ◽  
Author(s):  
E. Steinberger ◽  
G. Duckett
Keyword(s):  
Pituitary Gland ◽  
Leydig Cell ◽  
Testosterone Propionate ◽  
Follicle Stimulating Hormone ◽  
Inhibitory Effect ◽  
Blood Levels ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
Marked Drop ◽  
Stimulating Hormone

ABSTRACT On the basis of a study of changes in follicle stimulating hormone (FSH) levels in rat pituitary glands, obtained at various times after orchiectomy, it has been previously suggested that the Leydig cell secretions may regulate the release of FSH from the pituitary gland (Steinberger & Duckett 1966). This hypothesis was put to test in the present study. FSH levels have been determined in the pituitary gland and plasma of normal, testosterone-treated, orchiectomized, and orchiectomized testosteronetreated rats. A marked drop of pituitary FSH levels, associated with an elevation of plasma FSH levels, was observed in orchiectomized rats. Administration of testosterone to orchiectomized rats prevented the drop in pituitary FSH levels and rendered the blood levels undetectable. These results are interpreted as supporting the hypothesis that testosterone has an inhibitory effect on the release of FSH from the pituitary gland.

ONSET OF OESTROGEN-INDUCED PROLACTIN SECRETION AND DNA SYNTHESIS BY THE RAT PITUITARY GLAND

1977 ◽  
Vol 72 (1) ◽  
pp. 35-39 ◽  
Author(s):  
JOAN JACOBI ◽  
H. M. LLOYD ◽  
J. D. MEARES
Keyword(s):  
Dna Synthesis ◽  
Pituitary Gland ◽  
Prolactin Secretion ◽  
Male Rat ◽  
Serum Prolactin ◽  
Rat Pituitary ◽  
The Times ◽  
Pituitary Prolactin

SUMMARY The times of onset of oestrogen-induced prolactin secretion and DNA synthesis were studied in the pituitary gland of the male rat. At intervals from 3 to 96 h after injection of 10 mg diethylstilboestrol dipropionate, serum and pituitary prolactin concentrations were measured by radioimmunoassay and pituitary DNA synthesis by incorporation of [3H]thymidine in vitro. Serum prolactin was raised significantly from 6 h onwards and DNA synthesis was increased from 30 h onwards. Pituitary prolactin concentration began to increase at 30 h. Significant correlations were obtained between serum prolactin and DNA synthesis from 24 to 72 h but not during the period of prolactin secretion from 6 to 24 h.

Hypothalamic dopamine and catechol oestrogens in rats with spontaneous pituitary tumours

1983 ◽  
Vol 96 (2) ◽  
pp. 347-352 ◽  
Author(s):  
R. A. Prysor-Jones ◽  
J. J. Silverlight ◽  
J. S. Jenkins
Keyword(s):  
Pituitary Gland ◽  
Plasma Prolactin ◽  
Pituitary Tumours ◽  
Dopamine Concentration ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
Normal Rat ◽  
Old Rats ◽  
Hypothalamic Dopamine

Dopamine concentration within the hypothalamus and its depletion after the administration of α-methyl-para-tyrosine were measured in young rats and compared with values obtained in aged animals with and without spontaneously occurring pituitary tumours. Old rats had significantly reduced hypothalamic dopamine concentrations and there was less depletion of dopamine compared with young animals but there were no differences between tumorous and non-tumorous animals. Hyperprolactinaemia induced in young animals caused a much greater depletion of hypothalamic dopamine than in old tumorous rats with comparable plasma prolactin concentrations. The catechol oestrogen 2-hydroxyoestradiol inhibited the release of prolactin from normal rat pituitary glands in vitro but measurement of catechol oestrogens in the hypothalamus showed no differences between young and old tumorous or non-tumorous rats. It is concluded that reduced dopamine concentration and an impaired response to hyperprolactinaemia in old rats may facilitate the growth of prolactin-secreting tumours arising in the pituitary gland.

Regression of redundant lactotrophs in rat pituitary gland after cessation of lactation

1986 ◽  
Vol 111 (3) ◽  
pp. 367-NP ◽  
Author(s):  
E. S. Haggi ◽  
A. I. Torres ◽  
C. A. Maldonado ◽  
A. Aoki
Keyword(s):  
Pituitary Gland ◽  
Cell Count ◽  
Morphometric Analysis ◽  
Morphological Changes ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
Prolactin Content ◽  
Prolactin Synthesis ◽  
Regressive Changes

ABSTRACT Regressive changes occurring in the pituitary gland of the rat after removal of litters were studied. Pituitary glands of lactating rats were characterized by the presence of numerous hypertrophied lactotrophs. Interruption of lactation caused a blockade of prolactin synthesis and secretion, followed by degeneration of lactotrophs. Morphometric analysis of pituitary glands revealed that lactotrophs accounted for about 50% of the total hypophysial cell count in lactating rats. This percentage decreased progressively and reached pre-pregnant levels 7 days after removal of litters; the decrease was inversely correlated with an increase in the number of degenerating lactotrophs which comprised 30% of all lactotrophs 72 h after removal of litters. The morphological changes found in lactotrophs were closely related to changes in the prolactin content of serum and the pituitary gland. Regression of lactotrophs appeared to be the most important cause inducing the reversal of hypophysial lactotrophic activity to pre-pregnant conditions. J. Endocr. (1986) 111, 367–373

The involvement of ovarian factors in maintaining the pituitary glands of female rats in a state of low LH responsiveness to LHRH

1987 ◽  
Vol 112 (2) ◽  
pp. 265-273 ◽  
Author(s):  
J. de Koning ◽  
A. M. I. Tijssen ◽  
G. P. van Rees
Keyword(s):  
Pituitary Gland ◽  
Phase Response ◽  
The Self ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Lag Phase ◽  
Second Phase ◽  
Rat Pituitary ◽  
Pituitary Glands

ABSTRACT The effects of discontinuation and restoration of ovarian influences on the pituitary LH response to LHRH in vitro were investigated. When female rat pituitary glands taken on day 2 of dioestrus were incubated with LHRH the release of LH was low during the first hour (lag phase response) and afterwards a progressive, protein synthesis-dependent increase took place (second phase response), this being the self-priming action of LHRH. Short-term discontinuation (less than 1 day) of ovarian influences on the rat pituitary gland in vivo (ovariectomy) or in vitro (incubation in medium only) resulted in an increased LHRH-induced LH response during the lag phase. The biphasic LH response or the self-priming action of LHRH disappeared completely after long-term discontinuation of ovarian influences on the pituitary gland, LH release being at its maximum from the start of the incubation. The biphasic response was reinstated when ovaries were implanted under the kidney capsules of ovariectomized rats. Auto-implantation of an ovary into the spleen immediately after bilateral ovariectomy did not, however, prevent the disappearance of the LHRH self-priming action. Ovarian activity responsible for the presence of the low LH response during the lag phase was thus effectively removed by the liver, but inhibin-like activity suppressing serum FSH levels remained present. Silicone elastomer implants (s.c.) containing oestradiol-17β, implanted for 4 weeks, did not reverse the loss of the biphasic LH response to LHRH. It is concluded that liver-labile factors released by the ovaries keep the pituitary gland in a state of low responsiveness to LHRH. By giving a sufficiently high LHRH stimulus this inhibitory effect is neutralized and transition to a highly responsive state can be achieved. The ovarian factor(s) is not identical to inhibin or oestradiol-17β. J. Endocr. (1987) 112, 265–273

EFFECT OF 6-DEHYDRO-16-METHYLENE-HYDROCORTISONE AND DEXAMETHASONE ON THE RELEASE OF ACTH FROM RAT PITUITARY GLANDS IN VITRO

1970 ◽  
Vol 63 (3) ◽  
pp. 431-436 ◽  
Author(s):  
K. Berthold ◽  
A. Arimura ◽  
A. V. Schally
Keyword(s):  
Pituitary Gland ◽  
Direct Action ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
Acth Release

ABSTRACT Direct action of 6-dehydro-16-methylene-hydrocortisone (STC 407) and dexamethasone on the rat pituitary gland was investigated in vitro. CRF-induced ACTH release was suppressed after preincubation of the pituitary gland with 10 μg STC 407/ml or 1 μg dexamethasone/ml. These results suggest that both STC 407 and dexamethasone act directly on the pituitary gland.

Sign in / Sign up

Export Citation Format

Share Document