FOS EXPRESSION IN THE GONADOTROPIN-RELEASING-HORMONE (GNRH) NEURON DOES NOT INCREASE DURING THE OVARIAN STEROID-INDUCED GNRH SURGE IN THE RHESUS-MONKEY
Jw. Witkin et al., FOS EXPRESSION IN THE GONADOTROPIN-RELEASING-HORMONE (GNRH) NEURON DOES NOT INCREASE DURING THE OVARIAN STEROID-INDUCED GNRH SURGE IN THE RHESUS-MONKEY, Endocrinology, 135(3), 1994, pp. 956-961
The purpose of this study was to investigate the expression of the imm
ediate early gene, c-fos, in GnRH neurons in female rhesus monkeys as
a function of generation of the LH surge. Adult monkeys were either in
tact (n = 6) or ovariectomized (n = 10). Intact animals received estra
diol benzoate (EB; 330 mu g in oil, sc; n = 5) or oil (n = 1). Ovariec
tomized animals received either EB (n = 5) or EB, followed by progeste
rone (P; 2.5 ml in oil, im; n = 4), or oil (n = 1). Animals were kille
d from 31-75 h after EB treatment. Blood samples were collected to doc
ument LH release in response to steroid treatment. A surge of LH was i
nitiated in most animals that received EB alone or EB plus P about 30
h after steroid treatment. Animals were perfused with 4% paraformaldeh
yde, and brain blocks encompassing the region known to contain the maj
ority of GnRH neurons (septum through the medial basal hypothalamus) w
ere cut on the vibratome. Sites of FOS and GnRH immunoreactivities wer
e demonstrated using double labels with a variety of chromogens. Regar
dless of the time in the surge, there were very few GnRH neurons with
FOS immunoreactivity in their nuclei (0-9%). FOS-positive nuclei were
seen in many other neurons in various brain regions, including the sup
rachiasmatic and supraoptic nuclei. There were no differences in FOS e
xpression in GnRH neurons in intact and ovariectomized animals or in s
teroid- or oil-treated animals. These results suggest that FOS activat
ion in GnRH neurons is not associated with the initiation of the secre
tory GnRH stimulus to the LH surge in the rhesus monkey. If confirmed,
these data suggest that the GnRH nerve terminal may be the primary si
te for the control of the GnRH surge.