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.
Social isolation is one of the strongest predictors of increased risk of mortality in older adulthood. The ability to form and maintain the social relationships that mitigate this risk is partially regulated by the oxytocinergic system and one's ability to attend to and process social information. We have previously shown that an epigenetic change to the DNA of the oxytocin receptor gene (OXTR methylation) affects the salience of social information in young adults. Little is known about how the oxytocinergic system ages and what effect this aging system has on social cognitive abilities throughout the lifespan. Here we explore age-related differences in the association between neural response during selective social attention and OXTR DNA methylation in young and older adults. We find that older adults activate diffuse areas of visual cortex and dorsolateral prefrontal cortex during selective social attention, consistent with the dedifferentiation and compensatory neural activation commonly reported in aging. We find a significant age-by-OXTR methylation interaction on neural response when attending to social stimuli in a complex display; young adults display a positive association between OXTR methylation and neural activation, replicating our prior finding that young adults with presumed diminished endogenous access to oxytocin recruit regions of the attentional cortex to a greater extent. This association does not hold for older adults. Instead, perceived social support interacts with OXTR methylation to influence neural response during selective social attention. These data suggest that environmental factors like social support moderate biological processes in aging and highlight the importance of a lifespan perspective for understanding associations between individual differences in the oxytocinergic system, neural function, and social behavior.
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