The key to cot death may be a brain-signalling chemical that is better known for regulating mood, research has suggested.

Scientists have discovered the first direct evidence that an imbalance of serotonin in the brainstem can kill infant animals, offering insights into the origins of sudden infant death syndrome (SIDS), the leading killer of children aged under 12 months.

The findings, from experiments with genetically modified mice, add to a belief that serotonin is involved in many if not most human cot deaths. They build on the results of a study in 2006 that identified serotonin deficits in the brainstems of cot death victims, and show that a similar abnormality regularly kills mice of a similar age.

The new study, published in the journal Science, has also isolated a possible genetic cause of this imbalance. The abnormalities, however, could also be a result of environmental factors known to raise the risk of cot death, particularly parental smoking.

If the genetic link is confirmed, the research could lead to ways of identifying babies at risk, and to interventions that could reduce the danger. In Britain there were 380 unexplained deaths among infants aged under 2 in 2004. Cot death occurs in about one in 2,000 babies.

Enrica Audero, who led the research at the European Molecular Biology Laboratory in Monterotondo, Italy, said of the mouse model: “Ultimately, we hope it will give new ideas to doctors about how to diagnose babies at risk for SIDS.”

The 2006 research at Children's Hospital, Boston, compared postmortem brain samples from 31 cot death victims with tissue taken from 10 infants who had died of other causes. The cot death babies had a reduced ability to use and recycle serotonin in the brainstem, which controls critical unconscious functions, such as breathing, heart rate and temperature.

The discovery led scientists to suggest that a serotonin imbalance in the brainstem could cause death by preventing the detection of falling oxygen levels or rising body temperature. Babies might fail to wake as they normally would in response to such cues, causing them to suffocate. The danger would be particularly high among babies sleeping on their fronts - a known cot death risk factor.

Dr Audero's team engineered genetically modified mice to overproduce a serotonin regulator called Htrla, of which excessive levels have been found in some cot death victims.

Cornelius Gross, head of the laboratory's mouse biology unit, said the mice seemed normal at first, “but then they suffered sporadic and unpredictable drops in heart rate and body temperature. More than half of the mice eventually died of these crises during a restricted period of early life. It was at that point that we thought it might have something to do with SIDS.”

Most of the transgenic mice died before reaching three months. Only 30per cent survived beyond four months. Those that survived, however, had a normal lifespan, suggesting that there is a critical period for risk.

Further study showed that the mice were unable to regulate temperature, breathing or heart rate properly when subjected to certain kinds of stress. This is thought likely to influence their high risk of death in infancy.

George Haycock, of Evelina Children's Hospital in London and scientific advisor to the Foundation for the Study of Infant Deaths, said that more work was needed to establish the cause of the serotonin imbalance in cot death victims.

Dr Audero said that the team would examine whether it was possible to determine which of the serotonindefective mice were most likely to die.

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