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Serotonin Levels Tied to SIDS

Infants can't gasp and wake themselves up, researchers speculate

WEDNESDAY, March 8, 2006 (HealthDay News) -- While the exact cause of SIDS is unknown, a new study provides what researchers hope will be an important clue that could lead to screening, and perhaps new treatments, for the deadly syndrome.

In work done with brain stems from mice, researchers found out what happens when the brain's level of oxygen is depleted and the levels of the hormone serotonin are disturbed in so-called pacemaker cells.

These cells are a specific group of neurons that these same researchers have already shown to be responsible for gasping, which is needed to reset a normal breathing pattern in sleeping babies.

The researchers found that normal serotonin levels are needed for these respiratory pacemakers to induce gasping. It has been found that infants who die from SIDS -- sudden infant death syndrome -- have disturbed levels of serotonin. About 3,000 infants die each year from SIDS, and it is the primary cause of death for those under the age of 1, according to the U.S. Centers for Disease Control and Prevention.

The new report appears in the March 8 issue of the Journal of Neuroscience.

"When you have no oxygen, you shut down your respiratory network," explained study author Jan-Marino Ramirez, an associate professor of organismal biology and anatomy at the University of Chicago. "You rely on gasping as the only chance to wake up."

Others have shown that, with SIDS, infants gasp only one or two times and they don't wake up, Ramirez said. "We have shown that the nerve cells that you need for gasping need serotonin," he said.

In their experiments, Ramirez's team, knowing that serotonin regulates sodium channels in pacemaker cells, looked closely at serotonin levels in sodium-driven pacemaker neurons in the breathing center of the brain.

The researchers found that when they took serotonin away from these pacemaker cells, the gasping decreased from about 20 gasps to two or three -- not enough for the baby to wake up.

Ramirez believes that the mechanism they found in their mouse model will hold true for humans.

Identifying how gasping works may lead to new methods of screening and treating infants at risk for SIDS. "We might be able to link this to a better diagnosis," Ramirez said.

In addition, knowing how the gasping mechanism and its dependence on serotonin work may led to a better understanding of environmental factors, such as smoking, that appear to increase the risk of SIDS.

"We can ask about how the presence of nicotine changes the functioning of these cells," Ramirez said.

It is also possible that children who have altered serotonin levels may develop other problems later in life, such as depression, bipolar disorder or attention-deficit disorder, Ramirez said. "This find will lead to a better understanding of child development and SIDS," he said.

One expert thinks this study is in line with the current research on the causes of SIDS.

"There is growing evidence that most babies who die of SIDS have subtle defects in their abilities to control respiration," said Betty McEntire, executive director of the American SIDS Institute. "Studies such as this one are vital in helping to understand the root of the defect."

Breathing rhythms and the ability to gasp are developed in infants in the womb, McEntire noted. "Perhaps for some babies, this defect is related to reduced levels of serotonin and other brain chemicals," she said.

Another expert thinks this research sheds light on one possible aspect of the cause of SIDS.

"This is a very exciting result, and significantly extends our understanding of the mechanisms of gasping," said Dr. George B. Richerson, a professor of neurology, cellular and molecular physiology at Yale University.

Of course, the mice do not die of SIDS, so it is not clear exactly how gasping relates to SIDS, Richerson said. "It is not likely that SIDS is due just to a defect in gasping, but that would certainly contribute to the lack of recovery of an infant exposed to a severe stressor," he said.

"However, there is evidence that a defect in gasping is a part of the pathophysiology of some cases of SIDS. There is also good evidence that there is a defect in the serotonin system of infants that have died of SIDS. Thus, this mouse work nicely ties together these two bodies of work," he said.

More information

The National Institute of Child Health and Human Development can tell you more about SIDS.

SOURCES: Jan-Marino Ramirez, Ph.D., associate professor, organismal biology and anatomy, University of Chicago; Betty McEntire, Ph.D., executive director, American SIDS Institute, Marietta, Ga.; George B. Richerson, M.D., Ph.D., professor, neurology, cellular and molecular physiology, Yale University, New Haven, Conn.; March 8, 2006, Journal of Neuroscience
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