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New research sheds light on the molecular basis of crib death
Date:7/3/2008

d organs involved in temperature regulation such as brown fat tissue. This signalling is defective in the mouse model of SIDS. For example, when placed into a cold chamber the animals cannot properly activate brown fat tissue to produce heat. This inability to activate fundamental body systems under certain conditions is likely to explain why the mice succumb to sudden death.

While a complete block of serotonin signalling does not lead to death, upsetting its intricate balance by overexpressing serotonin 1A autoreceptor can. In response to serotonin the receptor initiates a negative feedback mechanism that reduces serotonin release and dampens down the signal to the body. The researchers caution, however, that it is unlikely that the exact same molecular mechanism leads to SIDS in humans. Nevertheless, the mouse model will help to shed light on how serotonin signalling, when dysfunctional, can be life-threatening.

"We hope the mouse model will help identify risk factors for SIDS. One open question is whether like in SIDS, the animals die during sleep and whether we can identify which mice will die by looking at their heart rate or body temperature before the crisis. Ultimately, we hope it will give new ideas to doctors about how to diagnose babies at risk for SIDS," says Enrica Audero, who carried out the research in Gross' lab.


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Contact: Anna-Lynn Wegener
wegener@embl.de
49-622-138-7452
European Molecular Biology Laboratory
Source:Eurekalert

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