Scientists Provide New Evidence for Cellular Cause of SIDS
Sudden Infant Death Syndrome
University of Chicago researchers and colleagues have found strong support that a disturbance of a specific neurochemical can lead to sudden infant death syndrome, the primary cause of death before age 1 in the United States. Approximately 3,000 infants die each year from SIDS, according to the Centers for Disease Control and Prevention.
In the March 8, 2006, issue of the Journal of Neuroscience, researchers describe what happens during hypoxia when levels of the hormone serotonin are disturbed in pacemaker cells - the specific group of neurons they previously showed to be responsible for gasping, which resets the normal breathing pattern for babies. Scientists found that normal serotonin levels are needed in these respiratory pacemakers to induce gasping and ignite auto-resuscitation.
"This confirms our previous studies," said Jan-Marino Ramirez, one of the authors of the study and professor of organismal biology and anatomy. "Now we've just better defined the players in the system."
In a paper published last year in the journal Neuron, Ramirez's work found that sodium-driven pacemaker cells controlled gasping. This work in tissue slices was confirmed in a study published last month by University of Bristol researchers who found the same results in rats.
Scientists knew that sudden infant death syndrome (SIDS) victims had disturbed levels of serotonin in areas critical for respiration. Since serotonin regulates the sodium channels in pacemaker cells, Ramirez's research team examined more closely serotonin levels in sodium-driven pacemaker neurons in the breathing center.
When researchers removed serotonin from these pacemaker cells, the gasping drastically decreased, from typically about 20 gasps to just two or three gasps - not enough for the baby to awaken.
"It indicates that if there's a problem with serotonin, the gasping is gone," Ramirez said. "And when these children don't gasp, they don't wake up."
According to the researcher, when the body senses a lack of oxygen, it shuts down most of the cellular respiratory network and focuses its energy on gasping, which is modulated solely by sodium-driven pacemaker neurons. If that specific neuron is blocked, for whatever reason, the body cannot gasp.
This means there may be nothing wrong with a baby's breathing under normal conditions, but if the baby goes into hypoxia from a blocked airway or because the baby sleeps on its tummy and does not receive sufficient oxygen, the child needs the sodium-driven pacemakers in order to gasp, which wakes the baby and initiates movement or crying.
"Gasping is an important arousal or auto-resuscitation mechanism," Ramirez said. It resets a baby's normal breathing rhythm and also alerts the baby as well as the mother that something is wrong.
"During normal breathing, it's a complicated network. However, the network becomes more vulnerable to situations like hypoxia, because under these conditions, respiration relies on only one group of pacemakers that become the critical drivers of [breathing] rhythm," Ramirez said.
Disturbed serotonin levels are also implicated in many psychiatric conditions, such as depression, bipolar disorder and attention deficit disorder. According to Ramirez, adults suffering with these types of conditions may be survivors of sudden infant death syndrome.
Ramirez and his colleagues now are looking more closely at the effects of different levels of serotonin, as well as the hormone norepinephrine, and exactly how much of each is necessary to keep auto-resuscitation in tact.
This study was funded by a grant from the National Institutes of Health. Other authors of the paper are: Andrew Tryba of the Medical College of Wisconsin, first author, and Fernando Pena of Departamento de Farmacobiologia, Cinvestav-Coapa, Mexico, co-author.