CHANGES IN PULSATILE RELEASE OF NEUROPEPTIDE-Y AND LUTEINIZING-HORMONE (LH)-RELEASING HORMONE DURING THE PROGESTERONE-INDUCED LH SURGE IN RHESUS-MONKEYS
Mj. Woller et E. Terasawa, CHANGES IN PULSATILE RELEASE OF NEUROPEPTIDE-Y AND LUTEINIZING-HORMONE (LH)-RELEASING HORMONE DURING THE PROGESTERONE-INDUCED LH SURGE IN RHESUS-MONKEYS, Endocrinology, 135(4), 1994, pp. 1679-1686
In previous studies we have shown that the pulsatility of LH-releasing
hormone (LHRH) release in gonadectomized monkeys is modulated by inpu
t from neuropeptide-Y (NPY) neurons: 1) the endogenous release of NPY
in the stalk-median eminence (S-ME) was pulsatile; 2) NPY pulses were
temporally correlated with LHRH pulses, with NPY pulses preceding LHRH
pulses by approximately 5 min; and 3) infusion of NPY into the S-ME s
timulated LHRH release, whereas 4) infusion of antiserum to NPY suppre
ssed endogenous LHRH pulses. It is not known, however, whether ovarian
steroid hormones alter the pulsatility of NPY and LHRH release or whe
ther the temporal correlation of NPY and LHRH pulses is maintained dur
ing the LH surge. In the present study we examined the changes in puls
atile release of NPY and LHRH in ovariectomized monkeys treated with e
stradiol benzoate (EB) followed by progesterone or oil. Using push-pul
l perfusion, perfusate samples from S-ME were collected at 10-min inte
rvals for 15 h. NPY and LHRH concentrations in the perfusates were mea
sured by RIA. Circulating LH levels were also monitored by periodic bl
ood sampling and RIA. Injection of progesterone (sc) after EB induced
an LH surge with a peak latency of 7.3 +/- 1.3 h (mean +/- SE) in seve
n of seven monkeys, whereas oil injection after EB elicited an LH surg
e in none of seven monkeys. The progesterone-induced LH surge was asso
ciated with an increase in LHRH release; the mean, pulse amplitude, an
d pulse frequency increased significantly (for all, P < 0.05) 4-8 h af
ter progesterone. NPY pulse frequency also increased significantly (P
< 0.05) 4-8 h after progesterone treatment, whereas mean release and p
ulse amplitude did not change in response to progesterone. Oil treatme
nt after EB administration did not alter any parameter of LHRH and NPY
pulses. Interestingly, the NPY and LHRH pulses were highly correlated
(P < 0.001) in monkeys treated with either EB-progesterone or EB-oil,
and NPY pulses preceded LHRH pubes by 4.8 +/- 0.7 and 5.1 +/- 0.6 min
, respectively. In summary, 1) an episode of increased LHRH release oc
curs before and during the progesterone-induced LH surge; 2) accelerat
ion of LHRH pulse frequency and the increase in LHRH pulse amplitude a
fter progesterone are accompanied by acceleration of NPY pulse frequen
cy; and 3) ovarian steroids do not affect the temporal correlation bet
ween NPY and LHRH pulses. These results suggest that modulation of NPY
pulse frequency by ovarian steroids may be a signal to stimulate LHRH
pulses during the progesterone-induced LH surge. Collectively, these
data suggest that NPY neurons play an important role in the modulation
of LHRH pulsatility and in the feedback effects of ovarian steroids.