Abstract

Neural circuits are shaped by experience during periods of heightened brain plasticity in early postnatal life. Exposure to acoustic features produces age-dependent changes through largely unresolved cellular mechanisms and sites of origin. Here, we isolated the refinement of auditory thalamocortical connectivity by in vivo recordings and day-by-day voltage-sensitive dye imaging (VSDI) in an acute brain slice preparation. Passive tone-rearing modified response strength and topography within mouse primary auditory cortex (A1) during a brief, three-day window but failed to alter tonotopic maps in the thalamus. Gene-targeted deletion of a forebrain-specific, cell-adhesion molecule (Icam5) accelerated plasticity in this critical period. Consistent with its normal role to slow spinogenesis, loss of Icam5 induced precocious stubby spine maturation on pyramidal cell dendrites in neocortical layer 4 (L4), identifying a primary locus of change. The evolving postnatal connectivity between thalamus and cortex in the days following hearing onset may thus determine a critical period for auditory processing.

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