Intercellular communication within the rat anterior pituitary gland. III. Postnatal development and periodic changes of cell-to-cell communications in female rats

1991 ◽  
Vol 231 (3) ◽  
pp. 351-357 ◽  
Author(s):  
Tsuyoshi Soji ◽  
Hisanori Nishizono ◽  
Takashi Yashiro ◽  
Damon C. Herbert
1975 ◽  
Vol 65 (2) ◽  
pp. 177-182 ◽  
Author(s):  
C. E. McCORMACK ◽  
W. F. STRAUSS

SUMMARY In immature female rats injected with PMSG at 30 days of age (day 30), ovulation occurs between the hours of 02.00 and 03.00 on day 33. If progesterone is injected at 10.00 h on day 32, the onset of ovulation is advanced by 1–2 h. In rats that were not given progesterone, ovulation was blocked by phenobarbitone sodium administered on day 32 before 13.50 h. However, pretreatment with progesterone at 10.00 h caused ovulation to occur in spite of phenobarbitone treatment at 13.50 h. An early release of ovulatory gonadotrophin from the anterior pituitary gland cannot completely account for progesterone's capacity to reverse the blockade of ovulation by phenobarbitone, because when phenobarbitone treatment was advanced by 2–4 h, ovulation still occurred in most progesterone-treated rats.


2004 ◽  
Vol 287 (4) ◽  
pp. E767-E771 ◽  
Author(s):  
D. Pisera ◽  
M. Candolfi ◽  
S. Navarra ◽  
J. Ferraris ◽  
V. Zaldivar ◽  
...  

Tissue homeostasis results from a balance between cell proliferation and cell death by apoptosis. Estradiol affects proliferation as well as apoptosis in hormone-dependent tissues. In the present study, we investigated the apoptotic response of the anterior pituitary gland to lipopolysaccharide (LPS) in cycling female rats, and the influence of estradiol in this response in ovariectomized (OVX) rats. The OVX rats were chronically estrogenized with implanted Silastic capsules containing 1 mg of 17β-estradiol (E2). Cycling or OVX and E2-treated rats were injected with LPS (250 μg/rat ip). Apoptosis was determined by the terminal deoxynucleotidyl-mediated dUTP nick-end labeling (TUNEL) method in sections of the anterior pituitary gland and spleen. Chronic estrogenization induced apoptosis in the anterior pituitary gland. Acute endotoxemia triggered apoptosis of cells in the anterior pituitary gland of E2-treated rats but not of OVX rats. No differences were observed in the apoptotic response to LPS in spleen between OVX and E2-treated rats. The apoptotic response of the anterior pituitary to LPS was variable along the estrous cycle, being higher at proestrus than at estrus or diestrus I. Approximately 75% of the apoptotic cells were identified as lactotropes by immunofluorescence. In conclusion, our results indicate that estradiol induces apoptosis and enables the proapoptotic action of LPS in the anterior pituitary gland. Also, our study suggests that estrogens may be involved in anterior pituitary cell renewal during the estrous cycle, sensitizing lactotropes to proapoptotic stimuli.


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