Results from previous studies indicate that abnormal patterns of release of LH pulses during the follicular phase of the menstrual cycle of women (either more or less frequent than normal) result in luteal phase deficiency and infertility. Development of a normal CL may depend on a healthy preovulatory follicle with adequate numbers of granulosa cells before ovulation, granulosa cells capable of synthesizing adequate quantities of progesterone, and adequate populations of LH receptors in the granulosa and the-ca cells. LH modulates its own receptor population in regulation of luteal function. Inadequate numbers of LH receptors in both granulosa and theca cells due to the absence of LH pulses before the preovulatory surge of LH may account for the smaller luteal structure in females in which release of LH was inhibited 48 h before the LH surge.
Alternatively, the smaller luteal structure of females in which episodic LH release was inhibited starting 48 h before the preovulatory surge of LH could have resulted from altered populations of luteal cells. In cattle and sheep, granulosa cells from ovarian follicles develop into large luteal cells, while small luteal cells are derived from theca cells. Angiogenesis is an important aspect of early development of the CL, but in vitro studies indicate that the angiogenic activity of CL of sheep is not controlled by LH stimulation. Eventually, small luteal cells of thecal origin may differentiate into large luteal cells during the late stages of CL development.