Improper regulation of serotonin triggered sudden death in mice, researchers report,,
THURSDAY, July 3 (HealthDay News) -- A malfunction in the regulation of the brain chemical serotonin may be at the root of sudden infant death syndrome (SIDS), new research suggests.
Reporting in the July 4 issue of Science, Italian researchers explain how alterations in normal serotonin levels in a mouse model resulted in sudden death for many of the mice. And, just prior to death, the mice experienced changes in their heart rate and their temperature that were similar to the changes suspected to occur in SIDS.
"This mouse model is important. Causing dysfunction in brainstem serotonin can lead to death in a majority of affected animals," Marian Willinger, a SIDS expert with the U.S. National Institute of Child Health and Human Development, said at a press conference Thursday. She added that the severe cardiac and thermal regulation changes that occurred in the mice are similar to risk factors associated with SIDS. For example, she said, stomach sleeping is more likely to cause heart rate variability than back sleeping. Over-bundling babies, and thus overheating them, is also a known risk factor for SIDS, she said.
The Italian researchers didn't set out to develop a mouse model of SIDS; they were originally looking at the serotonin system and how the body maintains its levels of the important neurotransmitter. But when many of the mice unexpectedly died, a scientist who was involved with SIDS research pointed out the similarities.
The brain's serotonin system works similar to a home thermostat, study author Cornelius Gross, from the European Molecular Biology Laboratory in Monterotondo, Italy, explained at the press conference. "When the heat rises past a set point, the heating is shut off. Serotonin has the same type of feedback," he noted.
The mouse model developed by Gross and his colleagues essentially contains a switch that they can turn on and off. This switch tells the mouse body to overexpress a serotonin receptor. In turn, that causes negative feedback that tells the mouse brain to reduce serotonin levels.
Serotonin is a neurotransmitter -- a chemical messenger -- that helps the brainstem communicate with nerve cells in the spinal cord and beyond. It is involved in many critical body functions, such as heart rate regulation, breathing, temperature regulation and more.
Interestingly, a complete block of serotonin doesn't cause death. "Having a dysfunction in the serotonin system is somehow worse than having no serotonin at all," Gross said.
These findings could lead to new ways to identify which babies are at the greatest risk of SIDS, said Gross. Both Gross and Willinger said they don't foresee a time when a pharmacological intervention could be developed to prevent SIDS, however.
"Drug therapy is probably not the way to do this. These neurotransmitters control a huge number of functions," said Willinger.
But, "if you could identify which babies are at risk, you could be a little more specific in who you insist make behavioral changes and modifications," said Dr. Rachel Moon, a pediatrician and SIDS researcher at Children's National Medical Center in Washington, D.C.
"Some babies are more at risk, and these environmental factors could overwhelm the baby's capabilities," added Moon, who is also a member of the American Academy of Pediatrics' SIDS Task Force.
To learn more about preventing SIDS, visit the U.S. National Institute of Child Health and Human Development.
SOURCES: Cornelius Gross, Ph.D., group leader, European Molecular Biology Laboratory, Monterotondo, Italy; Marian Willinger, Ph.D., National Institute of Child Health and Human Development, Bethesda, Md.; Rachel Moon, M.D., pediatrician and SIDS researcher, Children's National Medical Center, Washington D.C., and member, American Academy of Pediatrics Task Force on SIDS; July 4, 2008, Science
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