New Haven, Conn. -- Neurons thought to play a key role in sudden infant death syndrome (SIDS) are located near some of the largest arteries in the brain, according to a study by a Yale School of Medicine research team published in this week’s issue of the journal Nature Neuroscience.
The senior investigator, George Richerson, M.D., associate professor of neurology and physiology, said his team’s findings support a new theory that infants who succumb to SIDS have developmental abnormalities in these neurons. In healthy infants and adults, the response of these neurons to low carbon dioxide levels during sleep may alert them to wake and breathe deeply.
"When someone falls asleep with their face in a pillow, carbon dioxide levels rise," Richerson said. "The normal response is to wake up slightly, turn the head, and breathe harder. There is evidence that some infants that die of SIDS lack this normal protective response."
SIDS is the unexpected and sudden death of an apparently healthy infant during sleep. It is the leading cause of death in infants between two weeks and one year of age, striking about one per 1,000 infants. The cause is unknown, but certain risk factors have been identified, among them: lying face downward, prematurity, low birth weight, male sex, winter months and recent mild upper respiratory infection. A leading theory is that SIDS is a problem with breathing during sleep.
Breathing is dependent on normal levels of carbon dioxide, which is monitored by neurons in the brain called central chemoreceptors. Richerson and his co-investigators had established in earlier research that neurons in the brain containing the chemical serotonin are strongly stimulated by an increase in carbon dioxide, indicating that they are central chemoreceptors.
Carbon dioxide is the colorless, odorless gas given off from the lungs as a waste product of respiration. If carbon dioxide levels in the blood become either too high or too low, there are severe, even fatal, deleterious effects. Carbon dioxide levels within the blood are controlled within the normal range by changes in the depth and rate of breathing.
In this study, using imaging and electron microscopy, the researchers were able to show in laboratory rats that serotonergic neurons are located right next to large arteries in the brain, where they are ideally situated for sensing carbon dioxide levels in arterial blood. Thus, their location is optimized for their function as chemoreceptors.
Richerson said researchers at Harvard and Dartmouth who studied the brains of infants who died of SIDS found abnormalities of serotonin-containing neurons. "These are the same neurons that we have been studying in rats," he said. "We now believe that serotonin neurons play an important role in detecting a rise in carbon dioxide during sleep and they cause arousal and increased breathing. A defect in these neurons could lead to SIDS by preventing this normal response, resulting in death from excessive carbon dioxide levels."
Richerson said he and his team are collaborating with the scientists at Harvard and Dartmouth to understand how an abnormality of serotonin neurons could cause SIDS. "The ultimate goal," he said, "is to find a way to predict which children are at greatest risk, and find ways to reduce the chance that they will suffer this devastating event."
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