Tl. Horvath et al., LACK OF GONADOTROPIN-POSITIVE FEEDBACK IN THE MALE-RAT IS ASSOCIATED WITH LACK OF ESTROGEN-INDUCED SYNAPTIC PLASTICITY IN THE ARCUATE NUCLEUS, Neuroendocrinology, 65(2), 1997, pp. 136-140
We have demonstrated that estrogen induces synaptic reorganization in
the hypothalamic arcuate nucleus of female rats during the ovarian cyc
le and proposed that estrogen-induced synaptic retraction plays a role
in the disinhibition of gonadotropin secretion that occurs during the
afternoon of proestrus. This so-called positive feedback of gonadotro
pins is developmentally determined. It is present in female rats and a
bsent in males. To confirm the role of the estrogen-induced synaptic r
etraction in positive feedback, we tested whether administration of es
trogen to male rats also fails to induce synaptic remodeling of the ar
cuate nucleus. Male and female rats were gonadectomized and studied as
follows. One month following gonadectomy, animals received either a s
ingle injection of estradiol (100 mu g/animal in sesame oil; 12 males
and 12 females) or vehicle (6 males and 6 females). Twenty-four hours
following injections, all animals in the vehicle-injected group and 6
animals of each sex in the treatment groups were sacrificed, while the
rest of the animals were killed 48 h following the hormone injections
(6 per group). As expected, quantitative electron microscopic analysi
s of the female arcuate nuclei revealed that compared to oil-injected
controls, estradiol induced drastic decreases in the overall synapse c
ounts by 24 h (121 +/- 10 vs. 74 +/- 5 synapses/1,000 mu m membrane; p
< 0.05). Synaptic counts had recovered to control levels by 48 h. On
the contrary, in males, estradiol treatment did not cause changes in t
he total synapse counts at either time. As a further control, the lack
of an estrogen-induced gonadotropin surge in long-term castrate males
was also confirmed. Our study confirmed that in males estradiol does
not alter the net synaptology of the arcuate nucleus or cause gonadotr
opin positive feedback. This is in clear contradistinction to females
which show both synaptic plasticity and gonadotropin-positive feedback
upon receiving exogenous or endogenous estrogen. The lack of estrogen
-induced synaptic plasticity may be an underlying mechanism in the abo
lishment of positive gonadotropin, feedback in developing males and th
e development of constant estrus in aging female rats.