Intraventricular Injection of Follicle-Stimulating Hormone (FSH) during Proestrus Stimulates the Rise in Serum FSH on Estrus in Phenobarbital-Treated Hamsters through a Central Nervous System-Dependent Mechanism*

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Abstract
The serum gonadotropin profiles of 4-day cycling rodents exhibit LH and FSH surges during proestrus (P) and a second release of FSH during estrus (E). Peak serum levels of FSH during P occur between 1500–1800 h; the estrous FSH release starts late in the evening of P and reaches maximal serum levels during the morning of E. To delineate the mechanisms that regulate the estrous FSH rise and elucidate the role of FSH in its own secretion, hamsters were given Phenobarbital (ip) during P to block the endogenous gonadotropin surges and were subsequently injected systemically (iv) or intraventricularly (icv) with purified preparations of FSH or LH at 1500 h on P. Blood samples were obtained at regular intervals throughout P until 0900 h on E, at which time the animals were killed, and anterior pituitaries and hypothalami were collected. Serum and pituitary FSH and hypothalamic gonadotropin-releasing hormone were measured by RIA. Intact, saline-injected, and hypophysectomized (hypox) FSH-injected animals served as controls. Phenobarbital-treated, intact, proestrous animals that were injected (iv) with saline during P showed a blunted release of FSH during E. In contrast, phenobarbital-treated, intact, proestrous hamsters injected (iv) with 8000 ng purified FSH snowed an increase in serum FSH during E. Hypox hamsters treated with 8000 ng FSH (iv) exhibited no such rise in serum FSH levels 8 h postinjection. Stereotaxic cannulation of the third ventricle and administration of 2 μl saline at 1500 h on P had no effect on the low serum FSH concentrations during P and E in phenobarbital-treated hamsters. Similarly, icv injection of 50 or 200 ng purified FSH had no effect. In contrast, icv injection of 1000 or 1600 ng FSH at 1500 h on P stimulated a sustained release of FSH that attained peak serum concentrations during the morning of E. This phenomenon was not observed when 1000 ng FSH were injected iv in phenobarbital-treated proestrous hamsters or icv in hypox hamsters. The systemic injection of 10,000 ng LH at 1500 on P induced an endogenous FSH release during E. In contrast, icv injection of LH, up to a dose of 1,500 ng, failed to elicit an increase in serum FSH, thus suggesting that the site of action of LH is not at the level of the central nervous system. The icv FSH doses that were capable of eliciting endogenous FSH release were also effective in increasing the anterior pituitary FSH concentration at 0900 h on E, presumably through an increase in synthesis of the hormone. Interestingly, the icv FSH doses that failed to stimulate FSH secretion elicited an increase in the hypothalamic gonadotropin-releasing hormone content at 9000 h on E compared with controls. These studies support the theory that the proestrous secretion of FSH is essential in the regulation of the estrous FSH rise and further suggest that one site of action of FSH in this phenomenon is at the level of the central nervous system involving a short loop positive feedback system.