Synapsin is selectively required for anesthesia-sensitive memory.
Odor-shock memory in Drosophila melanogaster consists of heterogeneous components each with different dynamics. We report that a null mutant for the evolutionarily conserved synaptic protein Synapsin entails a memory deficit selectively in early memory, leaving later memory as well as sensory motor function unaffected. Notably, a consolidated memory component remaining after cold-anesthesia is not impaired, suggesting that only anesthesia-sensitive memory [ASM] depends on Synapsin. The lack of Synapsin does not further impair the memory deficit of mutants for the rutabaga gene encoding the type I adenylyl cyclase. This suggests that cAMP signaling, through a Synapsin-dependent mechanism, may underlie the formation of a labile memory component.
Knapek
Stephan
S
Universität Würzburg, 97074 Würzburg, Germany.
Gerber
Bertram
B
Tanimoto
Hiromu
H
D000758:Anesthesia; D000818:Animals; D030801:Animals, Genetically Modified; D003080:Cold Temperature; D004330:Drosophila / Q000235:genetics / Q000502:physiology; D056228:Feedback, Sensory / Q000502:physiology; D006185:Habituation, Psychophysiologic; D007858:Learning / Q000502:physiology; D008568:Memory / Q000502:physiology*; D008570:Memory, Short-Term / Q000502:physiology; D012903:Smell / Q000502:physiology; D016704:Synapsins / Q000235:genetics / Q000502:physiology*
D016704:Synapsins