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Evidence of a Role for Follicle-Stimulating Hormone in Controlling the Rate of Preantral Follicle Development in Sheep

School of Human Development (B.K.C.), University of Nottingham, Nottingham NG7 2UH, United Kingdom; Division of Biological Sciences (Institute of Cell and Molecular Biology) (E.E.T), University of Edinburgh, Edinburgh EH9 3JR, United Kingdom; Department of Obstetrics and Gynaecology (D.T.B.), University of Edinburgh, Edinburgh EH3 9EW, United Kingdom; and School of Biosciences (R.W.), Sutton Bonington Campus, University of Nottingham, Leicestershire LE12 5RD, United Kingdom

Address all correspondence and requests for reprints to: Dr. Bruce K. Campbell, School of Human Development, Floor D East Block, Queens Medical Centre, University of Nottingham, Nottingham NG7 2UH, United Kingdom. E-mail: bruce.campbell{at}nottingham.ac.uk.

Autografting ovarian cortex results in the loss of growing follicles and elevated gonadotropins. This paradigm was employed to examine the effect of gonadotropins on preantral follicle development in sheep. Ovarian tissue was recovered at 1, 2, 3, and 4 months after grafting from ewes that were either hyper- (n = 12; untreated) or hypogonadotropic (n = 12; GnRH-agonist and estradiol implants).

Compared with the Hypo group, Hyper ewes had higher (P < 0.001) gonadotropins, had greatly enlarged grafts, had reestablished a normal follicular hierarchy 2 months earlier (P < 0.05), had higher (P < 0.05) levels of proliferating cell nuclear antigen expression in tertiary, preantral, and antral follicles, and had higher (P < 0.01) concentrations of inhibin A and estradiol. Compared with time zero controls, increases in the number of primary follicles and the rate of proliferation in primary and secondary follicles in both groups of autografts (P < 0.05) were also observed.

In conclusion, the results of this experiment provide the first evidence that gonadotropins can affect the rate of development of preantral follicles in vivo in a large monovulatory species. Furthermore data are presented to support the existence of a gonadotropin-independent intraovarian feedback loop regulating both the rate of primordial follicle initiation and primary and secondary follicle development.

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