“We discovered that the neural pathways that carry OT to its sites of action in the brain don’t mature until a few weeks after birth in rats,” Rinaman reported, “and we’ve also found that OT contributes to the well-known effect of dehydration to inhibit food intake in mature rats and mice, but not in baby rats.”
Now, she said “we (with University of Pittsburgh research colleagues Janet Amico and Regis Vollmer) have shown that ‘dehydration anorexia’ is virtually absent in mice that have been genetically engineered to eliminate OT.” That is, so-called OT-null mice ate their regular amount of food even when they were dehydrated, which normally reduces the amount eaten. This followed earlier work where the ability of dehydration to inhibit food intake in rats was attenuated by blocking central OT receptors.
“These and other findings support the view that OT is a key signaling peptide in hypothalamic control of adaptive responses to dehydration,” Rinaman said, as well as that “the hindbrain appears to be a key target region through which the effects of OT are exerted.”
Rinaman is speaking at the American Physiological Society’s 2005 Conference, “Neurohypophyseal Hormones: From Genomics and Physiology to Disease,” plus the latest developments toward clinical applications, July 16-20 in Steamboat Springs, Colorado.
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