Abstract

The experiment was designed to study which part of the brain, the extrahypothalamic or hypothalamic area, are most involved in the release of LH and FSH in prepuberal rats. Electrical stimulation (100Hz, 0.1msec, 100μA S. Q.) was applied for 30min (30 sec on and off) to the several regions of the brain through implanted electrodes, and pituitary or serum contents of gonadotropin were measured by radioimmunoassay. 1) Rats were stimulated on 27 days of age and killed immediately after the stimulation. Stimulation of the arcuate nucleus (ARC), suprachiasmatic nucleus (SC), medial preoptic area (MPO), medial amygdala (AMYG) and the hippocampus (HPC) elevated the pituitary LH and FSH. Marked increases of pituitary LH and FSH were observed in the rats stimulated at the ARC, SC and HPC, but there was less of an increase in the rats stimulated at the AMYG. Serum FSH increased only by stimulation of the HPC. 2) Rats were stimulated beginning at the same age for 3 days successively and killed immediately after the 3rd stimulation. The 3-day stimulation of the ARC, MPO, and AMYG elevated the pituitary LH, while that of the HPC induced neither increase nor decrease. Both pituitary and serum FSH were elevated by the 3-day stimulation of the AMYG and MPO, while these were depressed by the 3-day stimulation of the ARC. 3) Rats of the same age were injected with estrogen (estradiol bonzoate, 0.5μg s. c.) about 48 hr before the stimulation and killed immediately after the 1-day stimulation. The marked elevations of pituitary LH and FSH were observed 48hr after the estrogen priming. Either stimulation of the MPO or of the AMYG increased pituitary LH, pituitary FSH and serum FSH, while stimulation of the HPC did not increase these in the animals. Therefore, at the first stage of puberty, the HPC may start to stimulare the release of FSH which may, in turn, be responsible for the growth of ovaries and estrogen secretion. After the increase of circulatory estrogen occurs, the AMYG and/or a more non-specific widely spread area may accelerate the further release of FSH to bring the vaginal opening and the first ovulation; however, the mechanism of the latter is unknown.

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