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Developmental neuroplasticity and adversity-related risk for psychopathology

Neuropsychopharmacology (2024)Cite this article

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Cellular-level mechanisms that govern plasticity inform how adversity affects neurobehavioral development. Among these, myelination is an experience-dependent process that also contributes to attenuating neuroplasticity. In mice, acute stress triggers neuropeptide release that initiates the proliferation of oligodendrocyte progenitor cells and subsequent myelination of active neurons [2]. This molecular cascade might impact the risk for stress-related psychopathology by altering the myelin content of a circuit, accelerating the closure of a sensitive period, and contributing to individual differences in neural structure. Parvalbumin-expressing (PV+) inhibitory interneurons also regulate plasticity; their emergence signals sensitive period opening, and their eventual formation of perineuronal nets marks sensitive period closure. Early-life adversity can accelerate PV+ cell emergence in the basolateral amygdala in mice [3], underscoring the experience-dependent nature of sensitive period timing.

Large-scale developmental neuroimaging studies suggest that early-life adversity can also accelerate neurodevelopment in humans. High prenatal adversity predicts accelerated structure-function decoupling in middle childhood [4], and greater adversity exposure confers a more mature corticolimbic functional connectivity phenotype in adolescence [5]. In both studies, adversity-exposed youth with “accelerated” neural phenotypes displayed lower psychiatric symptoms, suggesting that experience-dependent shifts in neurodevelopmental tempo may represent an adaptive response to challenging environments in the short term. Further, youth living in more disadvantaged neighborhoods showed reduced intrinsic fMRI activity in association cortices, potentially reflecting accelerated regional development [6]. As decreases in intrinsic activity are linked with increases in intracortical myelin and may signal a reduction in plasticity consistent with attenuation of a sensitive period, it is possible that adversity-related changes in neurodevelopmental tempo may also encompass accelerated sensitive period timing.

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Fig. 1: Experiences such as adversity exposure (depicted as a lightning bolt) can impact the timing of sensitive periods.

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Acknowledgements

This work was supported by funding from National Science Foundation (NSF) CAREER Award (BCS-2145372), National Institutes of Health (NIH) Director’s Early Independence Award (DP5OD021370), Brain & Behavior Research Foundation (NARSAD) Young Investigator Award, Jacobs Foundation Early Career Research Fellowship, and the Society for Clinical Child and Adolescent Psychology (Division 53 of the American Psychological Association) Richard “Dick” Abidin Early Career Award and Grant to DGG; and a NSF Graduate Research Fellowship Program Award (NSF DGE-1752134) to LMS.

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  1. Department of Psychology, Yale University, New Haven, CT, USA

    Lucinda M. Sisk & Dylan G. Gee

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  1. Lucinda M. Sisk
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  2. Dylan G. Gee
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LMS and DGG conceptualized the manuscript; LMS drafted the manuscript; and LMS and DGG edited the manuscript.

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Correspondence to Dylan G. Gee.

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Sisk, L.M., Gee, D.G. Developmental neuroplasticity and adversity-related risk for psychopathology. Neuropsychopharmacol. (2024). https://doi.org/10.1038/s41386-024-01950-y

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