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Updated: Jul 3, 2026
Preterm EEG: A Multimodal Neurophysiological Protocol
Published on: February 18, 2012
Preterm birth accelerates the maturation of spontaneous and resting activity in the visual cortex
Isabelle F Witteveen1, Emily McCoy1,2, Troy D Holsworth1
1Department of Psychology, College and Graduate School of Arts and Sciences, University of Virginia, Charlottesville, VA, United States.
Insights
Preterm birth accelerates brain maturation, leading to altered neural activity and suppressed neuronal firing in infants and mice. This cross-species study reveals potential mechanisms for neurodevelopmental conditions linked to prematurity.
Area of Science:
- Neuroscience
- Developmental Biology
- Comparative Medicine
Background:
- Prematurity is a significant risk factor for adverse neurocognitive outcomes.
- Alterations in brain structure and electrical activity are observed in preterm infants, but underlying circuit mechanisms remain unclear.
- Understanding these mechanisms is crucial for addressing neurodevelopmental challenges associated with preterm birth.
Purpose of the Study:
- To investigate the electrophysiological activity and circuit mechanisms in the visual cortex of prematurely born infants and mice.
- To elucidate how preterm birth impacts cortical maturation and resting neural activity.
- To utilize a cross-species approach to identify conserved mechanisms of preterm birth-related neurodevelopmental changes.
Main Methods:
- Electroencephalography (EEG) was used to assess visual cortical activity in preterm and term infants.
- In vivo electrophysiology and immunohistochemistry were employed in preterm and term mice models.
- Analysis focused on the aperiodic EEG component (1/f slope), neuronal firing rates, and inhibitory circuit maturation.
Main Results:
- Preterm infants and mice exhibited an accelerated maturation of the aperiodic EEG component, characterized by a flatter 1/f slope.
- This flatter slope was associated with decreased spectral power in theta and alpha bands and suppressed neuronal firing.
- Preterm birth led to accelerated maturation of inhibitory circuits in the visual cortex of mice.
Conclusions:
- Functional cortical maturation is accelerated by preterm birth in both humans and mice, with birth acting as a critical checkpoint.
- Accelerated maturation of inhibitory circuits and altered resting neural activity represent potential mechanisms underlying neurodevelopmental changes after preterm birth.
- A cross-species approach is valuable for studying the neural circuit mechanisms of preterm birth-related neurodevelopmental conditions.
Abstract:
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.
