The paper

R.T. Dosumu-Johnson et al., “Acute perturbation of Pet1-neuron activity in neonatal mice impairs cardiorespiratory homeostatic recovery,” eLife, 7:e37857, 2018.

More than 2,000 infants die each year in the US from sudden infant death syndrome (SIDS). Studies have linked the condition, in which babies stop breathing while sleeping, with drops in the activity of serotonin-producing neurons in the brain. And while serotonin, a neurotransmitter, helps regulate breathing, the chemical’s connection to SIDS isn’t completely clear.

To explore this connection, Harvard Medical School geneticist Susan Dymecki and her colleagues genetically altered mice so that their Pet1-neurons, which produce serotonin, stopped working after the animals received an injection of a chemical called clozapine-N-oxide. When the researchers exposed the week-old mice to a nitrogen and carbon dioxide gas mixture to mimic asphyxia, the animals gasped less for air...

If the weakened gasping seen in the neurologically impaired mice turns out to be identifiable in human babies with a higher risk of SIDS, it could give doctors a potential diagnostic criterion, the authors note in the paper. And the results also could offer a mechanistic explanation for abnormalities seen in the serotonin neurons of babies who died of the disorder.

It’s still unclear whether SIDS stems from the acute inhibition of serotonin neurons. Kevin Cummings, a biomedical scientist at the University of Missouri who wasn’t involved in the study, is skeptical that that’s the case. Instead, data from the brains of human babies who have died from the condition suggest a longer-term dysfunction within the serotonin system. “The result for anyone studying these neurons in relation to SIDS is totally relevant and totally interesting,” Cummings says. “But, in terms of the etiology of SIDS, I think there’s still a bit of a question there.”

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