Reliability of cortical signal processing is driven by glutamate maturation and supports working memory development.

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ABSTRACT
Postmortem animal & human models indicate changes in excitatory (E, via glutamate; Glu) and inhibitory (I, via GABA) neurotransmitters (NTs) through adolescence suggestive of critical period plasticity supporting cognitive development. E/I balance would enhance cortical SNR as spontaneous, asynchronous firing shifts to evoked synchronous firing. How NT indices of age-related changes in E/I balance support enhanced SNR in humans, is not known.

We acquired EEG during auditory steady state (SS) and memory guided saccade (MGS) tasks, and 7T MRSI at rest from 148 subjects (10-30yo, 77 F). Evoked activity was quantified as the mean-squared amplitude from the auditory SS task in the 50-200ms following onset of the auditory cue, and spontaneous activity was measured as the average standard deviation of activity per trial. We used linear mixed-effects models to compare EEG measures to MRSI-derived measures of PFC GABA & Glu and to MGS data.

Age-related decreases were found in performance variability in the MGS task. The difference between evoked and spontaneous frontal EEG increased with age, driven by decreases in spontaneous activity, consistent with increased cortical SNR. Increased SNR was associated with the deviation of Glu levels from their age-adjusted mean in both the MPFC and DLPFC in adolescents. Finally, higher SNR was associated with less variable responses on the MGS task.

These findings provide evidence that SNR is enhanced in conjunction with increases in E/I balance supporting a model for critical period plasticity through adolescence supporting cognitive maturation.