Fig. 6.

GnIH cells are activated by sex steroid exposure. We pursued the role of GnIH in modulation of estrogen negative feedback because of the importance of this process in regulation of ovulation and the coordination of receptivity. Ovariectomized hamsters were injected with either estradiol (B and D) or oil vehicle (A and C) and killed either 3 (A and B) or 6 (C and D) h after injection. The percentages of double-labeled GnIH and FOS neurons were counted (F). In oil-treated controls, few GnIH cells expressed FOS (A and C), whereas robust expression of FOS was evident in GnIH cells after estradiol treatment (B and D). Because estrogen administration led to FOS expression in GnIH cells, it was necessary to see whether estrogen was acting on GnIH neurons or systems upstream. Double-label immunofluorescence was used to colabel GnIH cells and ERα. ERα is expressed in a subset of GnIH cells in female hamsters, suggesting direct actions of estradiol on GnIH cell activation (E).