Journal
NEURON
Volume 65, Issue 3, Pages 385-398Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2010.01.024
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Funding
- FRAXA Research Foundation
- Autism Speaks
- Brain Research Foundation
- MRC (UK)
- NIH/NIMH [T32MH067564]
- MRC [G0700967, G0601584] Funding Source: UKRI
- Medical Research Council [G0700967, G0601584] Funding Source: researchfish
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Alterations in sensory processing constitute prominent symptoms of fragile X syndrome; however, little is known about how disrupted synaptic and circuit development in sensory cortex contributes to these deficits. To investigate how the loss of fragile X mental retardation protein (FMRP) impacts the development of cortical synapses, we examined excitatory thalamocortical synapses in somatosensory cortex during the perinatal critical period in Fmr1 knockout mice. FMRP ablation resulted in dysregulation of glutamatergic signaling maturation. The fraction of silent synapses persisting to later developmental times was increased; there was a temporal delay in the window for synaptic plasticity, while other forms of developmental plasticity were not altered in Fmr1 knockout mice. Our results indicate that FMRP is required for the normal developmental progression of synaptic maturation, and loss of this important RNA binding protein impacts the timing of the critical period for layer IV synaptic plasticity.
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