Circuit and plasticity defects in the developing somatosensory cortex of Fmr1 knock-out mice

Ingrid Bureau*, Gordon M.G. Shepherd, Karel Svoboda

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

146 Scopus citations

Abstract

Silencing of the Fmr1 gene causes fragile X syndrome. Although defects in synaptic plasticity in the cerebral cortex have been linked to cognitive impairments in Fmr1 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 of Fmr1 ko mice. In 2-week-old Fmr1 ko mice, 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 that Fmr1 shapes sensory cortical circuits during a developmental critical period.

Original languageEnglish (US)
Pages (from-to)5178-5188
Number of pages11
JournalJournal of Neuroscience
Volume28
Issue number20
DOIs
StatePublished - May 14 2008

Keywords

  • Barrel
  • Cortex
  • Development
  • Network
  • Neuron
  • Plasticity

ASJC Scopus subject areas

  • Neuroscience(all)

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