Serotonergic raphe neurons within the medulla control respiratory and autonomic function. In vitro, these neurons can act as chemoreceptors, detecting small changes in CO2 and pH in the physiological range. In support of this proposed sensing role, George Richerson and colleagues report on page 401 of this issue that the processes of these neurons are closely apposed to arterial blood vessels. Thus, these processes are in a prime location to monitor the effectiveness of lung ventilation in the blood. Because sudden infant death syndrome has been attributed to an inability to counteract rises in blood CO2 during sleep with an appropriate respiratory response mediated by serotonergic pathways, these results support the suggestion that the syndrome may result from a developmental abnormality in serotonergic chemoreceptive neurons.

Using confocal imaging and electron microscopy, the authors examined the relationship between serotonergic neurons (green) and arterial blood vessels (red). Processes of the neurons were closely associated with the arterial vessel walls, in some cases less than one micron from the blood-containing lumen. Electrophysiological recordings confirmed that the serotonergic neurons in close proximity to arteries responded to changes in pH, an indirect measure of CO2 concentration. The chemosensitive neurons were most common throughout the midline of the medulla, which contains large arteries and few veins. Thus the local CO2 concentration in this region probably reflects arterial CO2 concentration that is relatively unaffected by local tissue metabolism.