US scientists believe nerve cells critical for gasping offer important clues to the cause of cot death.
More research is needed says a medical adviser
Dr Jan-Marino Ramirez and colleagues at the University of Chicago have found two brain cell pathways that drive breathing baby mice.
Normally, one pathway will compensate if the other is blocked, causing the baby to gasp to take in air.
Cot deaths may occur if both pathways become blocked for some reason, say the authors in the journal Neuron.
How we gasp
Normally, if a baby becomes short of oxygen for any reason they will gasp.
Dr Ramirez's team had previously shown a specific group of pacemaker neurons in the brain controlled gasping in baby mice.
They had thought all of the neurons communicated in the same way, via sodium channels.
However, when scientists used a drug that blocks sodium they found only some of the neurons stopped communicating.
According to Dr Raminez this meant there must be two pathways that instructions to make the baby gasp.
Dr Raminez's team set out to study how some of the neurons remained active.
When they added a calcium-blocking drug as well as the drug to block sodium, all of the neurons stopped communicating.
Having shown that two pathways existed, they examined how the neurons reacted to normal oxygen levels and low oxygen, also called hypoxia.
According to the researchers, if the body is short of air for any reason it shuts down other respiratory messages and focuses its energy on gasping.
This message is mainly relayed by the neurons that use sodium to communicate.
Under normal conditions and oxygen levels, if you knock out the sodium pathway the calcium pathway takes over and delivers the gasping message.
In hypoxia this does not happen. The body appears to rely completely on the sodium pathway to send the message.
If this becomes blocked, the baby does not gasp in the normal way.
Dr Ramirez said this meant there might be nothing wrong with a baby's breathing under normal conditions.
But if the baby goes into hypoxia - from a blocked airway or is sleeping on their tummy and not getting enough air - he or she will not gasp.
Dr Ramirez explained: "In [normal oxygen levels] it's a complicated network and if you take away one component the rhythm is apparently undisturbed.
"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 the rhythm," he said.
Dr George Haycock, medical adviser to the Foundation for the Study of Infant Deaths and consultant paediatrician at King's College Hospital, London said: "This is interesting research that might ultimately help explain why some babies die suddenly and unexpectedly.
But he said more research would be needed given that the work was carried out on mice.
"Even if this theory turns out to be correct then we would still need to find ways to use the research and identify living babies who have the impaired cells and who, according to this theory, are at an increased risk of sudden death," he said.
Professor Peter Helms, chairman of the scientific advisory committee of Sudden Infant Death Syndrome (SIDS) International, said: "It is not clear how this finding relates to the dramatic fall in SIDS associated with the "back to sleep" campaign and the failure of
continuous respiratory monitoring in identifying infants at risk.
"However any new information on the mechanisms underlying the control of breathing must be welcome and may provide further insights relevant to some infants at risk of SIDS."