Importantly, the impaired long-term memory and LTP consolidation deficits were associated with significantly altered spine dynamics in the adult Baf53b+/− het mice following TBS. It is generally considered that pCofilin marks spines undergoing activity-dependent actin reorganization and also show an expansion in spine size thought to underlie the maintenance of LTP24,42. Similarly, BAF53bΔHDhigh mice had reduced availability of thin spines, consistent with the post-synaptic impairments in long-term synaptic plasticity. In juvenile and mature hippocampus, it is generally considered that thin spines are those where afferent patterned stimulation induces structural and functional plasticity, leading to incorporation of AMPA-type glutamate receptor in the synapse and a conversion from a thin to a mushroom type spine8,24,25,43. The specific loss of thin spines may indicate a loss in the ability to respond to afferent patterned stimulation by functional and structural plasticity, namely, incorporation of AMPA-type glutamate receptor in the synapse, synapse growth and the conversion of a thin to a mushroom type spine24-27,43. Given that these spine changes occurred relatively early in life (by 3 weeks of age) may contribute to the more severe LTP phenotype observed in this line of mutant mice, more closely mimicking the deficits observed in individuals with intellectual disability.
