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Biology of Reproduction, Vol 20, 1159-1165, Copyright © 1979 by Society for the Study of Reproduction
1 Reproductive Endocrinology Program,
Department of Pathology,
The University of Michigan,
Ann Arbor, Michigan 48109 The LH and FSH receptor content in thecal and granulosa cells of large antral follicles was
measured by in vitro binding assays and in vivo autoradiography during the rat estrous cycle.
Specific binding of [125I]-hCG to granulosa cells increased from <1000 cpm/µg DNA on estrus,
metestrus and diestrus to 6000 CPM/µg DNA on proestrus. Specific binding of [125I]-hFSH to
granulosa cells was consistently between 2000 and 3000 cpm/µg DNA throughout the cycle.
Specific hCG binding to thecal cells also increased between diestrus and proestrus, while specific
hFSH binding to thecal cells was essentially nondetectable. The increase in LH receptors in large antral follicles from diestrus to proestrus could be correlated with an increased ability of these follicles to produce cyclic AMP and estradiol during in vitro
incubations with increasing concentrations (0.06-60 µg/ml) of oLH. Incubation of antral follicles
collected on metestrus, diestrus and proestrus with and without testosterone revealed a progressive
increase in both follicular aromatase activity and endogenous androgen production. It is concluded that in the presence of low and unchanging LH and FSH concentrations from
metestrus to proestrus large antral follicles become more responsive to LH. This responsiveness is
associated with an increase in LH receptors both in thecal and granulosa cells and increased production of estradiol. Although the hormonal stimulus for the increase in granulosa cell LH receptor
on proestrus is not known, it is suggested that increased follicular estradiol might play a pivotal
role.
Note:
ACKNOWLEDGMENTS
The authors wish to thank Dr. J. L. Vaitukaitis and
Dr. G. D. Niswender for providing the antisera and Dr.
L. E. Reichert for providing the human FSH. Research
was supported, in part, by NIH-HD-09110, a Program
Project Grant NIH-HD-08333 and a Ford Foundation
Training Grant 700-0635B.
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