Parent attention-orienting behavior is associated with neural entropy in infancy.

Parents use joint attention to direct infants to environmental stimuli. We hypothesized that infants whose parents provide more bids for joint attention will display a more complex neural response when viewing social scenes. Sixty-one 8-month-old infants underwent electroencephalography (EEG) while viewing videos of joint- and parallel-play and participated in a free play interaction. EEG data was analyzed using multiscale entropy, which quantifies neural variability. Free play interactions assessed parent alternating gaze, a behavioral mechanism for directing attention to environmental cues. We found a significant positive association between parent alternating gaze and neural entropy in frontal and central regions. These results suggest a relationship between parent behavior and infant neural mechanisms that regulate social attention, underlying the importance of parental cues in forming neural networks.

Parent attention-orienting behavior is associated with neural entropy in infancy.

Parents play a significant role in directing infant's attention to environmental stimuli via joint attention. We hypothesized that infants whose parents provide more bids for joint attention will display a more complex neural response when viewing social scenes. Sixty-one 8-month-old infants underwent electroencephalography (EEG) while viewing videos of joint- and parallel-play and participated in a parent-infant free play interaction. EEG data was analyzed using multiscale entropy, which quantifies moment-to-moment neural variability. Free play interactions were coded for parent alternating gaze, a behavioral mechanism for directing attention to environmental cues. We found a significant positive association between parent alternating gaze and neural entropy in frontal and central brain regions. These results suggest a relationship between parent behavior and infant neural mechanisms that regulate social attention, underlying the importance of parent cues in the formation of neural networks in infancy.

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

Prematurity is among the leading risks for poor neurocognitive outcomes. The brains of preterm infants show alterations in structure and electrical activity, but the underlying circuit mechanisms are unclear. To address this, we performed a cross-species study of the electrophysiological activity in the visual cortices of prematurely born infants and mice. Using electroencephalography (EEG) in a sample of healthy preterm (N = 29) and term (N = 28) infants, we found that the maturation of the aperiodic EEG component was accelerated in the preterm cohort, with a significantly flatter 1/f slope when compared to the term infants. The flatter slope was a result of decreased spectral power in the theta and alpha bands and was correlated with the degree of prematurity. To determine the circuit and cellular changes that potentially mediate the changes in 1/f slope after preterm birth, we used in vivo electrophysiology in preterm mice and found that, similar to infants, preterm birth results in a flattened 1/f slope. We analyzed neuronal activity in the visual cortex of preterm (N = 6) and term (N = 9) mice and found suppressed spontaneous firing of neurons. Using immunohistochemistry, we further found an accelerated maturation of inhibitory circuits. In both preterm mice and infants, the functional maturation of the cortex was accelerated, underscoring birth as a critical checkpoint in cortical maturation. Our study points to a potential mechanism of preterm birth-related changes in resting neural activity, highlighting the utility of a cross-species approach in studying the neural circuit mechanisms of preterm birth-related neurodevelopmental conditions.

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

Prematurity is among the leading risks for poor neurocognitive outcomes. The brains of preterm infants show alterations in structure and electrical activity, but the underlying circuit mechanisms are unclear. To address this, we performed a cross-species study of the electrophysiological activity in the visual cortices of prematurely born infants and mice. Using electroencephalography (EEG) in a sample of healthy preterm (N=29) and term (N=28) infants, we found that the maturation of the aperiodic EEG component was accelerated in the preterm cohort, with a significantly flatter 1/f slope when compared to the term infants. The flatter slope was a result of decreased spectral power in the theta and alpha bands and was correlated with the degree of prematurity. To determine the circuit and cellular changes that potentially mediate the changes in 1/f slope after preterm birth, we used in vivo electrophysiology in preterm mice and found that, similar to infants, preterm birth results in a flattened 1/f slope. We analyzed neuronal activity in the visual cortex of preterm mice (N=6 preterm and 9 term mice) and found suppressed spontaneous firing of neurons. Using immunohistochemistry, we further found an accelerated maturation of inhibitory circuits. In both preterm mice and infants, the functional maturation of the cortex was accelerated, underscoring birth as a critical checkpoint in cortical maturation. Our study points to a potential mechanism of preterm birth-related changes in resting neural activity, highlighting the utility of a cross-species approach in studying the neural circuit mechanisms of preterm birth-related neurodevelopmental conditions.