Abstract
Radiofrequency lesions were generated in the organum vasculosum lamina terminalis (OVLT) of ovariectomized rats in order to examine the relationship of LHRH in the OVLT to that in the median eminence (ME) and the possible role of the OVLT in the control of gonadotropin secretion. In the first experiment, OVLT destruction significantly decreased LHRH content, as measured by RIA, in blocks of tissue containing the OVLT and the ME at 1, 3, and 7 days after production of lesions but did not alter serum LH and FSH levels or pituitary gonadotropin content. In the second experiment, OVLT lesions similarly did not alter serum gonadotropins or the negative feedback effect of estrogen in the ovariectomized rats; however, the progesterone-induced gonadotropin surge was nearly abolished as a result of OVLT destruction. LHRH content was reduced in the region of the OVLT, in the ME, and in a zone between these two structures. Bilateral medial preoptic area lesions also did not alter the negative feedback effect of estrogen but markedly reduced the progesterone-induced LH and FSH surges in comparison with those seen in sham-operated and unoperated controls, albeit to a lesser degree than OVLT lesions. Medial septal lesions resulted in only a slight reduction in the surge. Preoptic and septal lesions did not alter tissue LHRH content in the areas examined. These results indicate that the LHRH-containing elements in the OVLT are not essential for the control of tonic gonadotropin secretion but play an important role in the progesterone-induced LH and FSH surges. Furthermore, destruction of the OVLT resulted in a decrease in tissue LHRH content in the ME. We hypothesize that a diffuse population of LHRH-producing cells exists throughout the septalpreoptic regions and that OVLT lesions destroy not only LHRHcontaining terminals but also LHRH-containing axons passing through the region of the OVLT en route to the ME. These results are consistent with the concept of dual regulatory centers for the control of LH and FSH secretion and suggest that LHRH is delivered to the ME by axonal transport.