Neural mechanisms underlying sensitive period plasticity: Evidence from sight recovery in humans

The mechanisms underlying sensitive period plasticity in the mammalian cortex are well-characterised in non-human animal models, but human evidence remains scarce. Individuals treated for dense bilateral congenital cataracts in early childhood or adulthood undergo a transient period of postnatal visual deprivation, making it possible to characterize neurophysiological consequences of delayed sensory experience in human development.
Using MRS and EEG in sight recovery and typically sighted individuals, I will present converging evidence for two candidate mechanisms underlying sensitive period plasticity: the development of an E/I balance, and the establishment of corticocortical projections. Alterations in the Glx/GABA+ concentration ratio and aperiodic EEG signals suggested a lower E/I ratio in the visual cortex alongside elevated broadband neuronal firing, consistent with the experience-dependent development of the E/I balance. Additionally, attenuated stimulus-evoked and resting-state occipital alpha power following sight recovery was consistent with impaired corticocortical feedback processing, with behavioural consequences persisting decades after sight restoration.
Together, these findings provide rare human evidence that early visual experience shapes both E/I balance and corticocortical feedback in the visual cortex, suggesting that disruption to these processes might underlie the long-term visual deficits that follow congenital deprivation.

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