Together, these results indicate that BAF53b has a critical role in long-term memory formation. Importantly, all BAF53b mutant mice (BAF53bΔHD and Baf53b+/− hets) have normal short-term memory, indicating that they can perform these tasks and that their deficits at 24hrs are due to a failure of learning and memory and not performance. These results also support the hypothesis that BAF53b is involved in regulating gene expression required for long-term memory, as short-term memory in these tasks is transcription-independent.
