The transgenic approach allowed us to avoid potential effects of expressing mutant BAF53blt, independent of its role in neuronal development. The rescue effect was specific to the hippocampus-dependents in long-term memory for hippocampus-dependent tasks (object location and contextual fear conditioning). In contrast, long-term memory for cued fear was normal in both lines. This suggests that the hippocampus may be more sensitive to alterations in BAF53b function, as cued fear memory is considered hippocampus-independent. BAF53b may also have a key role in cortex-dependent long-term memory as well considering that mutant BAF53b mice also exhibited impaired long-term memory for object recognition. When performed in this way the task mainly depends on the perirhinal and insular cortices indicating a potential role for BAF53b mediated gene expression in these cortical regions.
