Cellular site and molecular mode of synapsin action in associative learning.

Birgit Michels, Yi Chun Chen, Timo Saumweber, Dushyant Mishra, Hiromu Tanimoto, Benjamin Schmid, Olivia Engmann, Bertram Gerber

    Research output: Contribution to journalArticlepeer-review

    33 Citations (Scopus)

    Abstract

    Synapsin is an evolutionarily conserved, presynaptic vesicular phosphoprotein. Here, we ask where and how synapsin functions in associative behavioral plasticity. Upon loss or reduction of synapsin in a deletion mutant or via RNAi, respectively, Drosophila larvae are impaired in odor-sugar associative learning. Acute global expression of synapsin and local expression in only the mushroom body, a third-order "cortical" brain region, fully restores associative ability in the mutant. No rescue is found by synapsin expression in mushroom body input neurons or by expression excluding the mushroom bodies. On the molecular level, we find that a transgenically expressed synapsin with dysfunctional PKA-consensus sites cannot rescue the defect of the mutant in associative function, thus assigning synapsin as a behaviorally relevant effector of the AC-cAMP-PKA cascade. We therefore suggest that synapsin acts in associative memory trace formation in the mushroom bodies, as a downstream element of AC-cAMP-PKA signaling. These analyses provide a comprehensive chain of explanation from the molecular level to an associative behavioral change.

    Original languageEnglish
    Pages (from-to)332-344
    Number of pages13
    JournalLearning & memory (Cold Spring Harbor, N.Y.)
    Volume18
    Issue number5
    DOIs
    Publication statusPublished - 2011

    ASJC Scopus subject areas

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

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