ABOVE: SUSAN DYMECKI LAB, HARVARD MEDICAL SCHOOL
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 and were more likely to die than ...
