ADMINISTRATION OF LONG-TERM ESTRADIOL AND PROGESTERONE FOLLOWED BY PROGESTERONE WITHDRAWAL DOES NOT ALTER THE PLASMA OXYTOCIN SECRETORY RESPONSE TO CHOLECYSTOKININ OR THE PITUITARY OXYTOCIN CONTENT IN OVARIECTOMIZED RATS
Ja. Amico et al., ADMINISTRATION OF LONG-TERM ESTRADIOL AND PROGESTERONE FOLLOWED BY PROGESTERONE WITHDRAWAL DOES NOT ALTER THE PLASMA OXYTOCIN SECRETORY RESPONSE TO CHOLECYSTOKININ OR THE PITUITARY OXYTOCIN CONTENT IN OVARIECTOMIZED RATS, Endocrine research, 23(1-2), 1997, pp. 69-80
The hormone oxytocin (OT) is important for several pre- and postpartum
events, including uterine contractions at parturition, the induction
of maternal behavior, and milk ejection during nursing. During late pr
egnancy, OT mRNA is increased in the paraventricular nucleus (PVN) due
to high estrogen and declining progesterone levels. Administration of
sequential estrogen and progesterone to, followed by withdrawal of pr
ogesterone from, an ovariectomized rat also increases OT mRNA. However
, pituitary OT peptide is not affected. In the present experiment, we
determined if this steroid exposure alters peripheral OT secretion dur
ing a provocative stimulus to OT release, such as cholecystokinin (CCK
). Adult ovariectomized Sprague-Dawley rats were implanted on day 1 wi
th either estrogen or empty silastic capsules, on day 3 with progester
one or empty capsules, and on day 14 progesterone or empty capsules we
re removed. Forty-eight hrs after removal of the progesterone capsules
, plasma OT was measured before and after i.v. injection of 10 mu g/kg
of CCK. At the completion of the study, pituitary glands were removed
and OT peptide was measured. No significant differences were found be
tween the sham and hormone-treated animals either in their basal or CC
K-stimulated plasma OT levels or their pituitary content of OT peptide
. Although sequential exposure to estradiol and progesterone followed
by withdrawal of progesterone has been shown previously to increase PV
N OT mRNA, neither pituitary OT immunoreactivity nor basal and CCK-sti
mulated release of plasma OT is affected by this treatment. Although t
he mechanism of this steroid effect is not yet understood, our observa
tions suggest a unique action of gonadal steroids upon PVN OT neurons.