Synapsin is selectively required for anesthesia-sensitive memory

Stephan Knapek, Bertram Gerber, Hiromu Tanimoto

研究成果: Article査読

40 被引用数 (Scopus)

抄録

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.

本文言語English
ページ(範囲)76-79
ページ数4
ジャーナルLearning and Memory
17
2
DOI
出版ステータスPublished - 2010 2
外部発表はい

ASJC Scopus subject areas

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

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