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Gonadotropin requirements for dominant follicle selection in GnRH agonist-treated cows

Department of Animal Sciences,163 Animal Science Research Center, University of Missouri, Columbia, Missouri 65211, USA and ¹ Department of Veterinary Medicine and Surgery, University of Missouri, Columbia, Missouri 65211, USA

Correspondence should be addressed to H A Garverick; Email: garvericka{at}missouri.edu

A study was conducted to examine the effects of gonadotropins on ovarian follicular development and differentiation in GnRH agonist (GnRHa)-treated cattle. Holstein cows were allotted into two pre-treatment groups: controls (n = 5) and GnRHa-treated (n = 9). Ovaries were removed from control cows on day 5 following a synchronized estrus. Treatment with GnRHa resulted in follicular arrest at <5 mm. Following follicular arrest, GnRHa-treated cows received a constant infusion of FSH for 96 h (GnRHa/FSH), with a randomly selected subset receiving hourly pulses of LH in addition to FSH during the last 48 h of infusion (GnRHa/FSH + LH). At the end of infusion, ovaries were removed, follicles were counted and measured, and follicular fluid samples were collected from large follicles (>10 mm). Differences in expression of mRNA for LH receptor, FSH receptor, cytochrome P450 side-chain cleavage, 3ß-hydroxysteroid dehydrogenase, cytochrome P450 17-hydroxylase (P450c17) and cytochrome P450 aromatase were determined in large follicles using in situ hybridization. The number of large follicles did not differ between GnRHa/FSH-treated and GnRHa/FSH + LH-treated cows (P = 0.64), but was greater than control animals (P 0.004). Follicular fluid concentrations of estradiol-17ß and androstenedione were highest in GnRHa/FSH + LH-treated cows (P 0.04), intermediate in control cows, and lowest in GnRHa/FSH-treated cows. Hybridization intensity of P450c17 was greater in GnRHa/FSH + LH-treated versus control or GnRHa/FSH-treated cows (P 0.03). These results indicate that while FSH can support bovine follicular growth >10 mm, LH increases androgen production and expression of P450c17.

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