Formation of long-term memory is the basis for learned behavior in higher organisms. The cellular correlate of long-term memory is long-term potentiation (LTP), which requires transcription and cytoskeletal rearrangements downstream of activity-triggered Ca2+ signaling (Kandel, 2012). Epigenetic mechanisms have important roles in LTP, the most well-studied examples being histone modifications and DNA methylation (Alarcón et al., 2004; Cohen-Armon et al., 2004). The contribution of chromatin remodeling to memory formation remains largely unexplored, but a recent study provides evidence that the nBAF complexes have a role in this process (Vogel-Ciernia et al., 2013). Mice heterozygous for BAF53b, as well as mice expressing dominant negative form of BAF53b (BAF53ΔHD) in Camk2a+ forebrain excitatory neurons, have abnormal spine morphology and impaired synaptic plasticity. While the short-term memory of the mice is normal, they have deficits in various facets of long-term memory including object location, object recognition and contextual fear. Consistent with this, hippocampal slices from BAF53ΔHD-expressing animals exhibit short-term potentiation (STP) but are unable to consolidate LTP. RNA-seq analysis of the dorsal hippocampus reveals that BAF53b+/− mice misregulate a variety of genes following
