Can flies have impaired immediate memory but normal consolidated memory?

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Extensive research has identified several molecular and neuroanatomical mechanisms underlying short-lived and long-lasting memory in Drosophila. At the molecular level, the genetic pathway of memory formation derived from mutant research appears to occur sequentially. Studies of Drosophila mutants have so far appeared to support the idea that defects in short-term memory (STM) are always associated with long-term memory (LTM) impairment. At the neuroanatomical level, distinct memory traces are distributed partly independently. Whether memory phases can also be dissociated at the molecular level, however, has remained unclear.

The researchers used genetic dissection of rugose mutants to investigate molecular separation of STM and consolidated memory. The rugose gene encodes an evolutionarily conserved A-kinase anchor protein, and its mutants showed immediate memory defects when tested using aversive olfactory conditioning. Despite this defective immediate memory, two established components of consolidated memory—anesthesia-resistant memory and protein synthesis-dependent LTM—were both normal after 10-session massed and spaced training. The researchers also found that rugose genetically interacts with cyclic AMP-protein kinase A signaling during STM formation. Together with their previous finding that AKAP Yu specifically participates in LTM formation, these results suggest that memory phases can be dissociated at the molecular level through distinct AKAPs in Drosophila.