Development of Cortical Circuitry and Cognitive Function

TLDR

Studies in nonhuman primates have mapped the neural circuitry of delayed‑response function, revealing that the principal sulcus connects with parietal, limbic, caudate, superior colliculus, and premotor areas, and that understanding this circuitry can inform education and developmental disorders. Cortical connections begin forming by the second trimester, and synapse number and density rise sharply to exceed adult levels between 2–4 months postnatally before gradually declining to stable adult levels. Delayed‑response performance emerges at ~4 months, aligning with peak synaptic density, indicating that a critical synaptic mass is required for this function and that maturation depends on later synaptic pruning.

Abstract

Recent functional and anatomical studies in nonhuman primates have elucidated the basic neural circuitry underlying delayed-response function in adult nonhuman primates. Thus circuitry includes connections of the principal sulcus with other areas of parietal association and limbic cortex and projections to the caudate nucleus, superior colliculus, and other premotor centers. Anatomical tracing in primate fetuses and in monkeys at various stages of postnatal development indicates that these various classes of cortical connections begin to form by the second trimester of pregnancy. Electromicroscopic studies of the principal sulcus and other areas of cerebral cortex show that the number and density of synapses in the cortex increase rapidly, reaching and maintaining higher than normal adult values between 2 and 4 months postnatally, before slowly declining over a period of years to stable adult levels. The capacity to perform delayed-response and/or AB at short delays emerges around 4 months of age, coinciding with the end of the period of highest synaptic density in the principal sulcus. These findings suggest that a critical mass of cortical synapses is important for the emergence of this cognitive function, and that fully mature capacity may depend upon the elimination of excess synapses that occurs during adolescence and young adulthood. Knowledge of the neural basis of normal cognitive development may prove useful both to social and educational purposes as well as to understanding developmental disorders of cognition.