LH release in the hamster depends on an estrogen-sensitive 24-hr periodicity within the central nervous system. Castrate hamsters were used to investigate whether medial preoptic area (mPOA) lesions and hypothalamic deafferentation affected this estrogen-induced release of LH. Within 24 hr after the injection of estradiol benzoate (EB), ovariectomized hamsters released LH in response to 5, 10, or 50 µg but not to 1 µg. Bilateral interruption ofthe neural fibers between the mPOA and medial basal hypothalamus (MBH) blocked ovulation in theintact hamster and prevented the estrogen-induced LH surge, but unilateral deafferentation did neither. mall lesions in the mPOA produced the same results provided the lesions were bilateral and included the most ventral part of the mPOA. Animals with misplaced lesions where the mPOAwasdestroyed unilaterally continued to cycle before ovariectomy and released LH in response to EB afte ovariectomy. In castrate males, both EB and testosterone propionate (TP) depressed the levels of serum LH to those observed in intact males but failed to induce the release of LH, an indication that the hypothalamus in the male hamster, like that in other rodents, is incapable ofgenerating a cyclic stimulus for gonadptropin release. These data support the hypothesis that the estrogeninduced release of gonadotropin in the ovariectomized hamster is a response to the same neural stimulus that causes the preovulatory release of gonadotropin in proestrous animals. In both intact and ovariectomized females, the neural stimulus which triggers the LH surge requires intact neural connections between the mPOA and MBH. (Endocrinology95: 1367, 1974)
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Norman et al. (1974) studied this question.