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 lead author Jan-Marino Ramirez, a 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 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.