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Like a candle flame, our metabolism consumes oxygen and releases carbon dioxide (CO₂). Breathing removes the CO₂ and brings in fresh oxygen, ensuring that metabolism—and life— can continue. It is the buildup of CO₂ more than the lack of fresh oxygen that makes you feel a strong urge to inhale when you hold your breath—like when you swim the length of a pool underwater.

This involuntary breathing reflex occurs because the buildup of CO₂ from metabolism is sensed by a special group of nerve cells (neurons) in the brain. When these sensory neurons are activated by the increased CO₂, they signal to trigger a breath. This reflex is critical to keep you breathing, but its function can stop working properly in very young children, older adults and people with chronic obstructive pulmonary disorder (COPD). The body’s failure to sense and respond to elevated CO₂ is also believed to be the main cause of sudden infant death syndrome (SIDS).

Past research has found where these CO2-sensing neurons are in the brain, but scientists don’t know exactly how they sense and signal when CO₂ levels are too high. Understanding this is critical for developing treatments that prevent SIDS and other types of breathing failure.

Gary Mouradian, PhD, of the Medical College of Wisconsin and his colleagues presented research at the Experimental Biology conference in April in Orlando, Fla., about how these neurons respond to elevated CO₂ to activate breathing. They turned to a state-of-the-art technological method called Patch-seq that studies single neurons in the brain. The technology compares the action of cells that respond appropriately to rising CO₂ levels to cells that do not. Specifically, Patch-seq allows researchers to identify which RNA is responsible for the CO₂ response. RNA is the messenger molecule that tells cells to make proteins crucial to sensing and responding to CO2. Although more research is needed, these findings show that Patch-seq may be able to help scientists better understand the CO₂ sensing reflex.

In the future, medicines that specifically target these unique proteins to preserve the CO₂-sensing reflex may help put an end to SIDS and other diseases in which this important reflex fails.

Sandy Martin, PhD, is a professor in the department of Cell and Developmental Biology at the University of Colorado School of Medicine. Sandy served as a meeting blogger for Experimental Biology 2019.