Preterm birth accelerates the maturation of spontaneous and resting activity in the visual cortex.

Prematurity is among the leading risk factors for poor neurocognitive outcomes. Brains of preterm infants often show alterations in structure, connectivity, and electrical activity, but the underlying circuit mechanisms are unclear. Using electroencephalography (EEG) in preterm and term-born infants, we find that preterm birth accelerates the maturation of aperiodic EEG components including decreased spectral power in the theta and alpha bands and flattened 1/f slope. Using in vivo electrophysiology in preterm mice, we find that preterm birth mice also show a flattened 1/f slope. We further found that preterm birth in mice results in suppressed spontaneous firing of neurons in the primary visual cortex, and accelerated maturation of inhibitory circuits, as assessed through quantitative immunohistochemistry. In both mice and infants, preterm birth advanced the functional maturation of the cortex. Our studies identify specific effects of preterm birth on the spectral composition of the infant EEG, and point to a potential mechanism of these effects, highlighting the utility of our parallel approach in studying the neural circuit mechanisms of preterm birth-related brain injury.