In 17 beta-estradiol (E)-treated ovariectomized (OVX) rabbits, the coitus-i
nduced luteinizing hormone (LH) surge is only one fourth that in ovarian-in
tact rabbits. in this study, we determined the pattern of the coitus-induce
d gonadotropin release, i.e., LH and follicle-stimulating hormone (FSH), in
OVX + E animals without or with continuous 3-wk treatment of 20-alpha-hydr
oxypregn-4-en-3-one (20 alpha P), For positive and negative experimental co
ntrols, ovarian-intact rabbits were either mated or sham mated, respectivel
y. The pituitary hormones prolactin (PRL) and growth hormone (GH) were meas
ured to serve as collateral controls for gonadotropins. The addition of con
tinuous 20 alpha P in OVX + E does fail to stimulate a coitus-induced LH su
rge equal in magnitude and duration to the LH surge in ovarian-intact rabbi
ts. Postcoital levels of FSH were greater in OVX + E + 20 alpha P animals t
han those in OVX + E rabbits, Coitus induced a PRL surge in ovarian-intact
and OVX + steroid-treated females, but not in mated males, thereby suggesti
ng a gender difference in this neuroendocrine circuit. Neither coitus nor s
teroids altered plasma CH values in female or male animals. We conclude tha
t chronic administration of neither E nor E + 20 alpha P can restore full-s
cale gonadotropin surges in OVX rabbits, whereas replacement of one or both
of these steroids is sufficient for a coitus-induced PRL surge, Moreover,
the presented observation that activin stimulates hypothalamic gonadotropin
-releasing hormone (GnRH) release suggests a possible involvement of ovaria
n proteins in the production of a full-scale coitus-induced GnRH/LH surge.