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Role of RIM1α in short- and long-term synaptic plasticity at cerebellar parallel fibres

Author

Listed:
  • Michael Kintscher

    (Neuroscience Research Center, Charité-Universitätsmedizin Berlin)

  • Christian Wozny

    (Neuroscience Research Center, Charité-Universitätsmedizin Berlin)

  • Friedrich W. Johenning

    (Neuroscience Research Center, Charité-Universitätsmedizin Berlin)

  • Dietmar Schmitz

    (Neuroscience Research Center, Charité-Universitätsmedizin Berlin
    Cluster of Excellence Neurocure, Charité-Universitätsmedizin Berlin
    Bernstein Center for Computational Neuroscience Berlin
    Deutsches Zentrum für Neurodegenerative Erkrankungen in der Helmhotz-Gemeinschaft)

  • Jörg Breustedt

    (Neuroscience Research Center, Charité-Universitätsmedizin Berlin)

Abstract

The presynaptic terminals of synaptic connections are composed of a complex network of interacting proteins that collectively ensure proper synaptic transmission and plasticity characteristics. The key components of this network are the members of the RIM protein family. Here we show that RIM1α can influence short-term plasticity at cerebellar parallel-fibre synapses. We demonstrate that the loss of a single RIM isoform, RIM1α, leads to reduced calcium influx in cerebellar granule cell terminals, decreased release probability and consequently an enhanced short-term facilitation. In contrast, we find that presynaptic long-term plasticity is fully intact in the absence of RIM1α, arguing against its necessary role in the expression of this important process. Our data argue for a universal role of RIM1α in setting release probability via interaction with voltage-dependent calcium channels at different connections instead of synapse-specific functions.

Suggested Citation

  • Michael Kintscher & Christian Wozny & Friedrich W. Johenning & Dietmar Schmitz & Jörg Breustedt, 2013. "Role of RIM1α in short- and long-term synaptic plasticity at cerebellar parallel fibres," Nature Communications, Nature, vol. 4(1), pages 1-8, December.
    • Handle: RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms3392
    DOI: 10.1038/ncomms3392
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