Contributed by Nicole Weaver| 09 March, 2006  20:50 GMT
 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.
There is strong evidence linking a specific neurochemical to the onset of sudden infant death syndrome, or SIDS, according to research published in the
Journal of Neuroscience.
SIDS is the primary cause of death before one year of age in the United States, accounting for 3,000 infant deaths per year, based on statistics from the
Centers for Disease Control and Prevention.
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University of Chicago researchers and colleagues found that a disturbance in serotonin levels can interfere with the ability of a baby to gasp, a function that is necessary for auto-resuscitation when a lapse in the normal breathing pattern occurs.
"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."
Previously, scientists had identified a specific group of neurons called pacemaker cells that regulate gasping. That study is described in a paper published last year in the journal Neuron. Ramirez's work was confirmed in a study published last month by University of Bristol researchers who found the same results in rats.
Serotonin Critical for Respiration
Scientists already 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.
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 Needed for Auto-Resuscitation
"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 SIDS.
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 intact. |