Gonadotrophins are fundamental to the mechanisms regulating follicle status
and development. Follicles in the ovary are either quiescent or committed
to one of two pathways: growth or atresia. The requirement for gonadotrophi
ns by the follicles varies with development: committed follicles grow indep
endently of gonadotrophins (primarily FSH) until the late preantral stage w
hen antrum formation is contingent upon FSH. The involvement of estrogen in
regulating gonadotrophin secretion is well documented and while evidence f
or a local regulatory role of estrogen in the ovary mounts, an obligatory r
ole for estrogen in the folliculogenic process has not been established. Th
e availability of a wide range of gene-disrupted mice termed 'knockouts', i
s providing information relevant to the study of folliculogenesis. Mice def
icient in either estrogen or estrogen receptors, are infertile primarily du
e to either a block in folliculogenesis prior to antrum formation or as a c
onsequence of failing to ovulate. Blocking estrogen stimulated, post-recept
or molecules such as cyclin D2, severely retards granulosa cell proliferati
on and leads to infertility, although the contribution of estrogn in this m
odel is not so clear given that FSH also stimulates cyclin D2. Similar prob
lems dissociating the Poles of FSH and estrogen are evident with the FSH de
ficient animal models. Nevertheless, estrogen is clearly an important and p
robably obligatory regulator of folliculogenesis, especially in the post an
tral stage. The exact points in the folliculogenic process where estrogen e
xerts its principal effects remains to br:elucidated. (C) 1999 Elsevier Sci
ence Ireland Ltd. All rights reserved.