New finding refutes theory of reproductive behavior
The miracle of birth; how does it happen? A little differently than we thought,
according to a study in the Oct. 15 issue of Proceedings of the National
Academy of Sciences (PNAS), which sheds new light on the endocrine control
of normal maternal and sexual behavior. The study was conducted collaboratively
by Thomas Insel, director of the Yerkes Primate Research Center and professor
of psychiatry at Emory, and Martin Matzuk, professor of pathology at Baylor
College of Medicine.
As humans marvel at the wonders of birth, certain hormones are behind the
scenes, making it all happen. Until now, the hormone oxytocin was thought
to be the instigator of the birth process in mammals, enabling a pregnant
female to start uterine contractions during labor, to begin lactating, to
bond with her newborn, and in general, to behave maternally. It is the same
hormone believed responsible for sexual receptivity to begin with, both
male and female, and for the bonding behavior between the two (called pair-bonding).
Oxytocin also was postulated to play a vital role in male copulation and
In PNAS, however, Insel reports that in mice, oxytocin is in fact essential
only for nursing and not for other maternal behaviors. And surprisingly,
male mice deprived of oxytocin showed no decline in sexual function at all,
and no change in behavior. "Although oxytocin can affect many processes,
it is not vital for maternal or sexual behaviors in mice," said Insel.
So why, then, are receptors for oxytocin so prevalent in the uterus and
uterine wall at the time of birth? "One hypothesis," said Insel,
"is that oxytocin secreted either locally or from the brain can aid
in the induction of labor and parturition, but is not absolutely essential--probably
because other substances that stimulate contractions are more potent and
fundamental in the process." Another possibility, he said, is that
a similar substance may bind to identical oxytocin receptors, replacing
oxytocin function in the mice who are oxytocin-deficient.
Oxytocin is produced mainly in the hypothalamus and released from the pituitary
gland, the tiny knob-like structure tucked beneath the brain. From there
it is released into circulation. It is also made in the corpus luteum (the
"white body" formed in the ovary immediately after ovulation),
in the uterus, the placenta, the amniotic sac (surrounding the developing
embryo), and in males, the testis.
Insel and his group performed their experiment on "knockout" mice--animals
lacking the gene that codes for oxytocin, thanks to special genetic engineering
techniques. In mice that are denied oxytocin, induction of labor and parturition
proceed normally, though the mice fail to nurse their offspring. Post-partum
injections of oxytocin restore milk ejection and rescue the offspring. Recent
studies suggest that oxytocin "knockout" mice show deficits in
various other social behaviors, although maternal behavior remains intact.
It is possible that mutations are present in the human genes for oxytocin
(or oxytocin receptors) in women with nursing defects. "An analysis
of women or families with nursing defects would be a first step in determining
whether any such mutations are present in humans," said Insel. This
would explain why some women have a difficult time with nursing, while others
handle it with ease. If, after further study, some women are found to lack
a functional gene, oxytocin injections might enable them to nurse normally
if they so choose, and provide their babies with the added immunological
benefits of mother's milk.
to the December 9, 1996 contents page