Serotonin neurons in the mouse brainstem where aspects of breathing control occur Image credit: YoonJeung Chang (CC BY 4.0)
Our survival depends on our heart and lungs working together to supply our cells with oxygen and remove carbon dioxide waste. The brain coordinates this process by controlling the activity of the heart and lungs. Yet sometimes a person may experience an event called an apnea and briefly stop breathing. If this happens, oxygen levels in the body fall while carbon dioxide levels rise. This in turn triggers a recovery process called autoresuscitation, which includes a series of large breaths or gasps, and each gasp is accompanied by increased heart rate due to specialized parts of the nervous system. This response usually restores normal breathing.
Failure of autoresuscitation may underlie many cases of sudden infant death syndrome, or SIDS (also known as “cot death” or “crib death”). SIDS is the leading cause of death in young infants in the western world, and many infants who die from SIDS show abnormalities in the brain cells that produce a chemical called serotonin. Evidence suggests that serotonin helps control breathing. This raised the question: does the autoresuscitation recovery response rely on serotonin-producing neurons?
To find out, Dosumu-Johnson et al. used one-week-old mouse pups that had been genetically engineered to respond to an injected drug by rapidly inhibiting their serotonin neurons. These animals are about the same age in mouse terms as infants at greatest risk for SIDS (~2-4 months of age). Inhibiting serotonin neurons made it harder for the mouse pups to recover from artificially induced apneas. Although their heart rate showed largely normal recovery – at least at first – their breathing did not. They took fewer gasps, and were more likely to die following such episodes.
These findings shed new light on how young animals control their breathing and heart rate when mounting an autoresuscitation recovery from an apnea. The observed uncoupling of breathing and heart rate recovery responses suggests that different brain cells and circuits control the two. The results also suggest that abnormalities in the activity of serotonin neurons may make infants more susceptible to SIDS. As well as offering a possible explanation to families who have lost a child to SIDS, these findings could be used to develop screening tools to identify other infants at risk. They also point to potential cellular targets for drugs that could ultimately help prevent further cases.
