Changes in Pituitary Responsiveness to LH-RH during Puberty in the Female Rat: Initiation of the Priming Effect

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Abstract
Pituitary responsiveness was evaluated after a single or 2 consecutive i.v. injections of LH-RH [luteinizing hormone-releasing hormone] at the time of puberty in the female rat. A single injection of LH-RH (20 or 100 ng/100 g b.w. [body weight]) significantly elevated plasma LH levels in prepubertal rats (anestrous phase of puberty, A); the response became minimal in early proestrus (EP) prior to the preovulatory peak of gonadotropins. In contrast to the adult, this response barely increased on the preovulatory day (late proestrus, LP) when the decapeptide was injected at a time of day prior to the gonadotropin discharge. Once the preovulatory surge of gonadotropins had started, there was a clear increase in responsiveness to LH-RH. Response to LH-RH was low during the 1st day of vaginal opening (estrus) and during the 2nd and 3rd day after vaginal opening (diestrus). The FSH [follicle stimulating hormone] response to LH-RH was greater during estrus than at EP or LP. At a time prior to the preovulatory surge of LH [luteinizing hormone], the LH response to a 2nd injection of LH-RH administered 60 min after the initial injection was enhanced only during LP. When the 2nd injection of the neurohormone was given after the proestrous gonadotropin surge had started, the response was markedly enhanced. Uterine weight, used as an index of estrogen secretion, was low in A, increased significantly during EP and became maximum at LP, declining thereafter during estrus and diestrus. Ovulation usually occurred in the night prior to the day of vaginal opening. In spite of elevated estrogen levels, the pituitary LH response to LH-RH only increases around the time of puberty when endogenous release of the neurohormone presumably occurs to elevate plasma LH. This increase in LH-RH release, possibly brought about by the rising estrogen titers, can subsequently exert a priming effect on the gland, which enhances the LH response to a further exposure to the neurohormone.