The juvenile-peripubertal transition period in the female rat is associated with an ovarian-independent afternoon increase in the amplitude of plasma
luteinizing hormone (LH) pulses. To determine if the immature pituitary could be activated to cause
precocious puberty juvenile female rats were subjected for 4 days to a microprocessor-driven pulsatile
intravenous administration of
LH-releasing hormone (
LHRH) at a dose that produced a peripubertal pattern of LH release. To determine if the
LHRH neurons themselves could be prematurely activated to induce such a pattern of plasma LH, and hence lead to
precocious puberty, the neuroexcitatory
amino acid analog
N-methyl-DL-aspartic acid (NMA) was similarly administered. The time of puberty (vaginal opening and first ovulation) was advanced by both the
LHRH and NMA treatments, by 5 and 7 days, respectively. Ovarian weight and incidence of corpora lutea at first diestrus were similar in all animals regardless of treatment, but a juvenile
body weight was retained by the animals that underwent
precocious puberty. Therefore, just as the adenohypophysis can be driven by exogenous
LHRH to initiate puberty, the
LHRH neuronal system can be precociously activated by the episodic administration of an
excitatory amino acid analog that is known to interact with specific brain receptors. It is likely, therefore, that sexual maturation is limited by factors that lie further upstream in the hypothalamo-pituitary axis (e.g., the neuronal circuits that impinge upon
LHRH-producing neurons).