STEAMBOAT SPRINGS, Colorado (July 18, 2005) -- Maternal aggressive/protective behavior is recognized throughout mammalian species, especially during lactation. When hiking, we warn our kids not to approach bear cubs, or to get between a cub and the mother. While driving and you see a fawn, you know a doe can't be too far away and will run headlong to protect it.
The same neurohypophyseal (NH) hormone, oxytocin (OT), is responsible for both the physiological and behavioral changes, but the site of action is quite different. OT is released during parturition and in lactation not only from NH terminals into the bloodstream in order to support reproductive systems, but also within the brain, into the supraoptic nucleus (SON) and paraventricular nucleus (PVN), where it has marked behavioral impact.
OT release in the brain is involved with such reproductive events as "morphological plasticity, autoregulation of OT neuronal activity and promotion of maternal behavior, including maternal aggressive behavior to protect offspring," Inga D. Neumann of the University of Regensburg, Germany, notes. "Thus in lactating rats from a line bred for high-anxiety behavior, or HAB, OT release within both the central amygdala and the PVN was positively correlated with the level of maternal offensive behavior against an intruder." In addition, the lactating HAB dams display higher aggression and central OT release compared with a low-anxiety line.
Very importantly, along with the rise of maternal behavior during lactation, OT also reduces anxiety levels by regulating the responsiveness of the hypothalamic-pituitary-adrenal axis. "Getting aggressive is one thing, Neumann observes, "but if you need to attack a bigger animal, you also must lower your level of anxiety."
Next, Neumann and her research team tested what effect direct OT insertion into the brain of virgin female rats would have. They found that "driving up-regulation of OT receptor binding in the central amygdala, using adeno-associated viral vectors, reduced the level of anxiety and promoted social dominance behavior in virgin females."
A model to determine OT regulation at birth
Alison Douglas, from the University of Edinburgh, who collaborated with Neumann on the previous study, is presenting a paper at the same meeting. Douglas sought to understand "the physiological mechanisms of birth to explain perinatal clinical problems that mothers may have, such as preterm labor, which put mother and baby at risk." Specifically she and her team investigated the role of certain chemicals in the brain that control OT secretion and the birth process. They administered drugs "to target their action in the brain of rats while they were giving birth."
"Using this model, we can investigate the functions of various brain chemicals and the regulation of OT secretion which are involved in the physiological processes of reproduction," Douglas said. "Parallels with the central mechanisms controlling oxytocin neurons in lactation may also help explain problems of 'milk let-down', where the mother is unable to breast feed," Douglas added.
Neumann and Douglas are presenting at the American Physiological Society's 2005 Conference, "Neurohypophyseal Hormones: From Genomics and Physiology to Disease," and the latest developments toward clinical applications, July 16-20 in Steamboat Springs.
They also are participating in the symposium, "Central control of lactation," chaired by Bill Armstrong of the University of Tennessee School of Medicine, and Glenn Hatton, University of California, Riverside.
"Oxytocin release within the brain: physiological and behavioral consequences in lactation." Inga D. Neumann, Martin Waldherr, Daniela Beiderbeck and Oliver Bosch, Institute of Zoology, University of Regensburg, Germany; Alison J. Douglas, University of Edinburgh; Larry Young, Emory University. Funded by Volkswagen Foundation and DAAD (German academic exchange) (Neumann); NSF (Young), British Council (Douglas).
"Evaluation of the role of central noradrenaline in activating oxytocin neurons at parturition." Alison J. Douglas, Alex Gillies, Vicky Briam, Simone Meddle, Neuroendocrinology, Centre for Integrative Physiology, University of Edinburgh, Scotland. Funded by Wellcome Trust.
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