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The effect of frontal hypothalamic deafferentation on the release of LH and FSH was studied in ovariectomized rats. Frontal cuts were placed just in front of the arcuate nucleus, at the posterior border of the optic chiasma (RCS), at the level of the anterior commissure (POS) and in front of the optic chiasma (PCS). Animals with RCS and POS cuts showed vaginal smears with persistent cornification; the other groups had irregular cycles.

The concentrations of LH and FSH in the serum increased after ovariectomy in deafferentated animals, but after 4 weeks the levels were lower than in the animals without hypothalamic lesions except for the PCS group. The more caudally that the cuts were located, the lower were the concentrations of hormones in the serum. The injection of repeated doses of oestradiol benzoate resulted in a decrease in serum gonadotrophin of both rats without hypothalamic lesions and RCS rats. Although a greater decrease was observed in the lesioned than in the intact rats, it is believed that such an effect does not indicate an increased sensitivity of deafferentated animals to this steroid.

The stimulatory effect of progesterone on LH and FSH release was studied in ovariectomized rats primed with oestradiol benzoate. The responses were unchanged in PCS animals but failed to occur in POS and RCS rats. Measurement of the level of gonadotrophin-releasing hormone in frontal hypothalamic slices from RCS animals showed a decreased level behind the cut and an increased one in front of it, suggesting that perikarya located in front of the section were sending their axons to the mediobasal hypothalamus. It is believed that the blockade of the stimulatory effect on gonadotrophins by frontal hypothalamic deafferentation is due to the transection of these axons. Cuts placed immediately in front of the arcuate nucleus, however, permitted progesterone-induced gonadotrophin release because of incoming neurones containing gonadotrophin-releasing hormone, which end in structures immediately rostral to the cut. The results indicate that effects of both inhibitory and stimulatory ovarian steroid feedback are impaired by frontal hypothalamic deafferentation.