Studies on the Mechanism of Follicle-Stimulating Hormone-Induced Desensitization of Sertoli Cell Adenylyl Cyclase in Vitro1

1985 ◽  
Vol 32 (4) ◽  
pp. 916-924 ◽  
Author(s):  
F Le Gac ◽  
H Attramadal ◽  
T Jahnsen ◽  
V Hansson
Keyword(s):  
Adenylyl Cyclase ◽  
Sertoli Cell ◽  
Follicle Stimulating Hormone ◽  
Stimulating Hormone

Basement Membrane Increases G-Protein Levels and Follicle-Stimulating Hormone Responsiveness of Sertoli Cell Adenylyl Cyclase Activity*

Endocrinology ◽  
1991 ◽  
Vol 128 (2) ◽  
pp. 1167-1176 ◽  
Author(s):  
MARTIN DYM ◽  
SUPANYA LAMSAM-CASALOTTI ◽  
MENG-CHUN JIA ◽  
HYNDA K. KLEINMAN ◽  
VASSILIOS PAPADOPOULOS
Keyword(s):  
Basement Membrane ◽  
Adenylyl Cyclase ◽  
G Protein ◽  
Sertoli Cell ◽  
Follicle Stimulating Hormone ◽  
Cyclase Activity ◽  
Adenylyl Cyclase Activity ◽  
Protein Levels ◽  
Hormone Responsiveness ◽  
Stimulating Hormone

Characterization and Follicle Stimulating Hormone Activation of Sertoli Cell Cyclic AMP-Dependent Protein Kinases

Endocrinology ◽  
1977 ◽  
Vol 101 (5) ◽  
pp. 1358-1368 ◽  
Author(s):  
JOHN L. FAKUNDING ◽  
ANTHONY R. MEANS
Keyword(s):  
Cyclic Amp ◽  
Protein Kinases ◽  
Sertoli Cell ◽  
Follicle Stimulating Hormone ◽  
Dependent Protein ◽  
Stimulating Hormone

Inhibin Production by Primary Sertoli Cell-Enriched Cultures: Regulation by Follicle-Stimulating Hormone, Androgens, and Epidermal Growth Factor*

Endocrinology ◽  
1988 ◽  
Vol 122 (2) ◽  
pp. 717-725 ◽  
Author(s):  
PATRICIA L. MORRIS ◽  
WYLIE W. VALE ◽  
SCOTT CAPPEL ◽  
C. WAYNE BARDIN
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Sertoli Cell ◽  
Follicle Stimulating Hormone ◽  
Epidermal Growth ◽  
Enriched Cultures ◽  
Stimulating Hormone

236. Effects of long term recombinant rat follicle-stimulating hormone replacement on the restoration of spermatogenesis after chronic suppression of gonadotrophins in adult rats

2008 ◽  
Vol 20 (9) ◽  
pp. 36
Author(s):  
S. M. Ruwanpura ◽  
P. G. Stanton ◽  
D. M. Robertson ◽  
R. I. McLachlan ◽  
Y. Makanji ◽  
...  
Keyword(s):  
Sertoli Cell ◽  
Germ Cells ◽  
Follicle Stimulating Hormone ◽  
Inhibin B ◽  
Testis Weight ◽  
Adult Rats ◽  
Early Pachytene ◽  
Pachytene Spermatocytes ◽  
Stimulating Hormone

Follicle stimulating hormone (FSH) in short-term rat studies supports spermatogenesis at multiple levels, notably spermatogonial development. The role of FSH in supporting full spermatogenesis in rats is still in question as long-term studies have not been possible due the development of neutralising antibodies to heterologous FSH preparations. This study sought to assess the effects of a homologous recombinant rat FSH (rr-FSH) preparation on the long-term restoration of spermatogenesis. Adult rats were GnRH-immunised (GnRH-im) for 12 weeks then, administered an anti-androgen; flutamide (flut), alone or together with rr-FSH (8µg/rat/daily) for 56 days (1 spermatogenic cycle). Germ and Sertoli cell numbers were quantified using an optical disector stereological method. Testis weight, serum FSH and inhibin B and Sertoli cell nuclear volume were significantly reduced to 15%, 13%, 25% and 57% of controls respectively, following GnRH-im+flut treatment. GnRH-im+flut treatment reduced A/I spermatogonial, type B spermatogonial+preleptotene, leptotene+zygotene and early pachytene spermatocyte numbers to 28%, 68%, 50% and 19% (P < 0.001) of controls respectively, with later germ cells rarely observed. After FSH treatment, no significant affect on testis weight, serum FSH and inhibin B or Sertoli cell number were observed. However, rr-FSH treatment significantly increased numbers of A/I spermatogonia, leptotene+zygotene and early pachytene spermatocytes from 28 = >42%, 50 = >69% and 19 = >27% of controls, respectively, while no differences were observed in later germ cell types. rr-FSH also increased (P < 0.05) the volume of Sertoli cell nuclei from 57 = >66% of control. In conclusion, FSH is unable to support full rat spermatogenesis; however, FSH can partially support germ cells notably spermatogonia through to early pachytene spermatocytes, despite the absence of androgenic support.

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