The differing responsiveness of the anterior- and the middle-anterior hypothalamic area to estradiol benzoate implant: inhibition of compensatory ovarian hypertrophy.

Estradiol benzoate (E2) was chronically implanted, unilaterally or bilaterally, for about 30 days in the anterior (A-AHA) or the middle (M-AHA) portion of the anterior hypothalamic area (AHA) of unilaterally ovariectomized (ULO) and intact cyclic rats. E2 unilaterally implanted in the A-AHA partially blocked and bilaterally implanted totally blocked compensatory ovarian hypertrophy (COH) in response to ULO. E2 implanted in the M-AHA induced ovarian atrophy in ULO rats. In M-AHA E2 implanted rats, ovulation was completely inhibited, vaginal smears became persistently cornified, serum FSH was drastically suppressed to 23-24% of the estrous level, LH was unremarkably changed. These effects were less pronounced when the implant was place in the A-AHA, i.e., ovulation was partially blocked only with bilateral implantation, vaginal cycles were irregular, serum FSH was suppressed to 66% and 44% of the estrous level after unilateral and bilateral implantation, respectively, LH was rather unchanged. Uteri were neither atrophic whether the implants was placed in the A-AHA or in the M-AHA. In normal cyclic rats, the effects of E2 implantation in the two areas were similar to those observed in ULO rats, except that the effects were evident even after unilateral implantation since the brain had not been compensated. The results allowed to indicate a functional subdivision of the ventral AHA, at least into the A-AHA and the M-AHA. The M-AHA was experimentally elucidated to be more estrogen sensitive than the A-AHA for monitoring of serum FSH, and was suggested to be involved in the episodic secretion of FSH. The inhibitory effect of estrogen on COH may primarily be mediated through the M-AHA and secondarily through the A-AHA.