Circuit and Plasticity Defects in the Developing Somatosensory Cortex ofFmr1Knock-Out Mice

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Abstract
Silencing of theFmr1gene causes fragile X syndrome. Although defects in synaptic plasticity in the cerebral cortex have been linked to cognitive impairments inFmr1 knock-out(ko) mice, the specific cortical circuits affected in the syndrome are unknown. Here, we investigated the development of excitatory projections in the barrel cortex ofFmr1 komice. In 2-week-oldFmr1 komice, a major ascending projection connecting layer 4 (L4) to L3 (L4→L3), was defective in multiple and independent ways: its strength was reduced, caused by a lower connection probability; the axonal arbors of L4 cells were spatially diffuse in L2/3; the L4→L3 projection did not show experience-dependent plasticity. By 3 weeks, the strength of the L4→L3 projection was similar to that of wild type. Our data indicate thatFmr1shapes sensory cortical circuits during a developmental critical period.