Dendritic spine instability and insensitivity to modulation by sensory experience in a mouse model of fragile X syndrome

摘要: Fragile X syndrome (FXS) is the most common inherited form of mental retardation and caused by transcriptional inactivation X-linked fragile 1 (FMR1) gene. FXS associated with increased density abnormal morphology dendritic spines, postsynaptic sites majority excitatory synapses. To better understand how lack FMR1 gene function affects spine development plasticity, we examined formation elimination layer 5 pyramidal neurons in whisker barrel cortex Fmr1 KO mice a transcranial two-photon imaging technique. We found that rates over days to weeks were significantly higher both young adult compared littermate controls. The heightened turnover was due existence larger pool “short-lived” new spines than Furthermore, existing ones less sensitive modulation sensory experience mice. These results indicate loss leads ongoing overproduction transient primary somatosensory cortex. insensitivity alterations suggest developing synaptic circuits may not be properly tuned stimuli FXS.