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Effect of FSH Treatment on LH and FSH Receptors in Chronic Cystic-Ovarian-Diseased Dairy Cows^{1, 2,}

Washington State University^,4, Pullman 99164-6332

Abstract

This experiment was conducted to 1) determine whether chronic cystic-ovarian-diseased (CCOD) cows fail to respond to luteinizing hormone (LH) treatment because of a lack of adequate ovarian LH receptors and 2) determine the effect of follicle stimulating hormone (FSH) treatment on ovarian LH and FSH receptors in ovaries of CCOD cows. The CCOD cows were those that did not resume cyclic ovarian activity after repeated treatment with human chorionic gonadotropin (hCG) and(or) LH-releasing hormone (LHRH) and were considered chronic by veterinarians. Thirteen CCOD cows were purchased from producers; six of them were injected with 5 mg FSH twice daily for 3 or 5 d (TCCOD) and the remaining seven remained untreated. Seven control (noncystic) cows in the luteal phase of the estrous cycle were injected with Lutalyse approximately 48 to 50 h before slaughter so they would be in the follicular phase (FP) of the cycle at the time of slaughter. Analysis of serum and pituitaries showed no differences (P>.05) in mean concentrations of serum or pituitary LH and FSH or pituitary LHRH receptor concentration and affinity among FP, CCOD and TCCOD cows. Ovarian follicle wall concentrations of receptors for LH (3.2 ± .6; 13.0 ± 2.5; 22.4 ± 5.1 fmol/mg protein) and FSH (10 ± 2.6; 43 ± 7.2; 29 ± 6.7 fmol/mg protein) were lower (P<.05) in CCOD cows compared with FP and TCCOD cows, respectively. The same pattern was observed for concentrations of granulosa cell LH and FSH receptors. The follicular fluid estrogen-to-androgen (testosterone and androstenedione; E:A) ratio was >1 in seven of seven FP, <1 in six of seven CCOD and >1 in five of six TCCOD cows. Ovaries of CCOD cows lack LH and FSH receptors when compared with FP cows, and these receptor concentrations can be increased to normal levels by treatment with exogenous FSH.

¹ Scientific Paper No. 6986. College of Agr. and Home Econ. Res. Center, Washington State Univ., Pullman 99164. This research was supported by USDA Animal Health Grant No. 82-CRSR-2-1030 and the Washington Dairy Products Commission.

² The authors gratefully acknowledge Dr. G. D. Niswender, Colorado State Univ., Fort Collins, CO for the estradiol antiserum; Dr. A. Belanger, Lab. of Molec. Endocrinol., Quebec, Canada for the androstenedione and testosterone antiserum; Dr. L. E. Reichert, Jr., Albany Med. College, Albany, NY for the purified ovine LH and FSH; Dr. J. A. Dias, Albany Med. College for the FSH antiserum; The Center for Population Res. of the Natl. Inst. of Child Health and Human Dev. of the Natl. Inst. of Health for the purified hCG (CR-121); and NIAMDD for the purified human FSH.

³ Reprint requests: Dr. J. J. Reeves, Dept. of Anim. Sci., Washington State Univ., Pullman, WA 99164-6332.

⁴ Dept. of Anim. Sci.