Synapsin is selectively required for anesthesia-sensitive memory
- 1Universität Würzburg, 97074 Würzburg, Germany;
- 2Max-Planck-Institut für Neurobiologie, 82152 Martinsried, Germany
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.
Footnotes
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↵3 Corresponding author.
Email hiromut{at}neuro.mpg.de; fax 49-89-89950-119.
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[Supplemental material is available online at http://www.learnmem.org.]
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Article is online at http://www.learnmem.org/cgi/doi/10.1101/lm.1661810.
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- Received October 8, 2009.
- Accepted November 30, 2009.
- Copyright © 2010 by Cold Spring Harbor Laboratory Press
