Splicing of particular targets in response to memory formation is not without precedent. For example, the splicing of the Orb2A transcript is required for both associative appetitive and courtship suppression memory in Drosophila (Gill et al. 2017). There is also evidence that this phenomenon may be conserved across species, since contextual fear conditioning induces differential splicing in the hippocampus of mice (Poplawski et al. 2016). It is, therefore, conceivable that while splicing may occur during all forms of synaptic plasticity, the isoform targets may be specific to the type of memory formed. The broad implication of this prediction is that the molecular engram of memory within relevant cells uses transcriptional diversity to provide the cellular plasticity associated with the type of memory being formed. This cellular encoding is bolstered by the diversity of epigenetic changes caused by neuronal activity associated with memory formation. For example, activity-induced histone modifications caused a late-onset shift in Neurexin-1 splicing reduced the stability of memories (Ding et al. 2017). Our data suggest that alcohol can affect transcriptional events, and thus shape how context is encoded during formation of memories.
