A sparse population of inhibitory Sst-Chodl neurons in the mouse neocortex became active during low arousal and connected distant cortical regions. Selective activation was followed by the widespread synchrony characteristic of slow-wave sleep and made mice fall asleep sooner. The peer-reviewed experiment shows that the cortex can participate directly in sleep regulation; it does not establish a treatment or the same mechanism in humans.
The peer-reviewed study identified Sst-Chodl cells, marked by somatostatin and chondrolectin, as a sparse but long-range class of inhibitory neuron in the mouse neocortex. Single-cell anatomical reconstructions showed axons extending beyond their local surroundings into multiple cortical regions. The cells were mostly silent during active wakefulness but more active in low-arousal states including quiet wakefulness and slow-wave sleep.[1], [2]
Researchers stimulated Sst-Chodl cells carrying a light-sensitive protein while measuring cortical activity. Selective stimulation shifted neural activity across regions into a synchronized state resembling slow-wave sleep. Broader chemogenetic activation also reduced the time mice spent awake, increased both slow-wave and rapid-eye-movement sleep, and shortened the time before sleep began.[1], [2]
The experiments showed that long-range inhibitory cells did more than track sleep state: they could actively initiate synchronization across the cortex. That finding adds an intracortical circuit to the established subcortical mechanisms involved in regulating sleep. The work was conducted in mice, however, and did not show that the same cellular arrangement performs the same function in human sleep or can treat a sleep disorder.[1], [2]
