Luteinizing hormone release by cerebral cortex stimulation in rats

Depletion of ovarian ascorbic acid from highly luteinized ovaries from rats was used as an index of endogenous liberation of luteinizing hormone (LH). When, in such rats, 2 µl of hypertonic saline was injected in the cerebral cortex, significant depletion of ovarian ascorbic acid took place compared with control animals. This stimulus was equally effective in different areas of the cortex that were explored. The mere implantation of the needle gave the same results. Procaine, added at 5% concentration to hypertonic saline, completely blocked cortical stimulation. The same effect was obtained by subcutaneous injection of estradiol benzoate (50 µg) or progesterone (1 mg). In animals with constant estrus, elicited by suprachiasmatic lesion, the response to cortical stimulation was blocked, but not completely. In these animals, however, an intense depletion of ovarian ascorbic acid was obtained by electrical stimulation of the hypothalamus. In animals with constant estrus, induced by injection of testosterone on the 2nd day after birth, the response was also affected. It is concluded that stimuli starting from the cerebral cortex can reach the hypothalamus and induce release of LH.