The capacity of pig uterine tissues to recognize and respond to matern
al and conceptus signals determines whether pregnancy can be establish
ed and defines the environment in which embryonic and fetal growth occ
ur. Limits of uterine capacity may be defined genetically. However, th
e extent to which functional uterine capacity approaches genetic poten
tial may be determined in part, by the success of organizational event
s associated with growth, morphogenesis and cytodifferentiation of ute
rine tissues. It is important, therefore, that these events be identif
ied and evaluated with respect to their potential effect on adult uter
ine function. Histogenesis of the pig uterus begins prenatally, but is
completed postnatally. Transformation of the uterine wall from histoa
rchitectural infancy to maturity occurs between birth and day 120. Mor
phogenetic events characteristic of the first 60 days of neonatal life
proceed normally in gilts ovariectomized at birth. These events inclu
de appearance and proliferation of uterine glands, development of endo
metrial folds, and growth of the myometrium. Endometrial development d
uring this period involves alterations in patterns of epithelial and s
tromal DNA synthesis, coordinated changes in the distribution and bios
ynthesis of extracellular matrix glycosaminoglycans and cell surface g
lycoconjugates, and specific alterations in patterns of uterine protei
n secretion. The ovary-independent, spatially coordinated nature of th
ese events suggests that neonatal uterine development is regulated loc
ally via dynamic cell-cell and cell-extracellular matrix interactions.
The extent to which such potentially critical interactions must be pr
eserved to ensure developmental success remains unknown. However, the
normal pattern of ovary-independent cellular and molecular events asso
ciated with development of the uterine wall was disrupted by treating
neonatal gilts with oestradiol valerate, and daily administration of o
estrogen to gilts from birth to day 13 did not affect ovulation rate,
but did reduce embryonic survival by 22% on day 45 of gestation in adu
lts that were exposed to oestrogen neonatally. These observations supp
ort the idea that some organizational events associated with developme
nt of the neonatal uterine wall must be allowed to proceed without int
erruption to ensure that adult uterine function is not compromised. Ef
forts to identify specific developmental determinants of uterine capac
ity may be facilitated by examining the consequences of xenobiotically
induced interruption of uterine development on adult uterine function
. Such studies may also contribute to identification of uterine factor
s affecting embryonic survival and fetal growth.