Synapsin is selectively required for anesthesia-sensitive memory

Stephan Knapek, Bertram Gerber, Hiromu Tanimoto

Research output: Contribution to journalArticlepeer-review

40 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)76-79
Number of pages4
JournalLearning and Memory
Volume17
Issue number2
DOIs
Publication statusPublished - 2010 Feb
Externally publishedYes

ASJC Scopus subject areas

  • Neuropsychology and Physiological Psychology
  • Cognitive Neuroscience
  • Cellular and Molecular Neuroscience

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