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Miniature neurotransmission is required to maintain Drosophila synaptic structures during ageing

Author

Listed:
  • Soumya Banerjee

    (EPFL - Swiss Federal Institute of Technology Lausanne)

  • Samuel Vernon

    (EPFL - Swiss Federal Institute of Technology Lausanne)

  • Wei Jiao

    (EPFL - Swiss Federal Institute of Technology Lausanne)

  • Ben Jiwon Choi

    (New York University)

  • Evelyne Ruchti

    (EPFL - Swiss Federal Institute of Technology Lausanne)

  • Jamshid Asadzadeh

    (EPFL - Swiss Federal Institute of Technology Lausanne)

  • Olivier Burri

    (EPFL - Swiss Federal Institute of Technology Lausanne)

  • R. Steven Stowers

    (Montana State University)

  • Brian D. McCabe

    (EPFL - Swiss Federal Institute of Technology Lausanne)

Abstract

The decline of neuronal synapses is an established feature of ageing accompanied by the diminishment of neuronal function, and in the motor system at least, a reduction of behavioural capacity. Here, we have investigated Drosophila motor neuron synaptic terminals during ageing. We observed cumulative fragmentation of presynaptic structures accompanied by diminishment of both evoked and miniature neurotransmission occurring in tandem with reduced motor ability. Through discrete manipulation of each neurotransmission modality, we find that miniature but not evoked neurotransmission is required to maintain presynaptic architecture and that increasing miniature events can both preserve synaptic structures and prolong motor ability during ageing. Our results establish that miniature neurotransmission, formerly viewed as an epiphenomenon, is necessary for the long-term stability of synaptic connections.

Suggested Citation

  • Soumya Banerjee & Samuel Vernon & Wei Jiao & Ben Jiwon Choi & Evelyne Ruchti & Jamshid Asadzadeh & Olivier Burri & R. Steven Stowers & Brian D. McCabe, 2021. "Miniature neurotransmission is required to maintain Drosophila synaptic structures during ageing," Nature Communications, Nature, vol. 12(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-24490-1
    DOI: 10.1038/s41467-021-24490-1
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    Cited by:

    1. Jamshid Asadzadeh & Evelyne Ruchti & Wei Jiao & Greta Limoni & Catherine MacLachlan & Scott A. Small & Graham Knott & Ismael Santa-Maria & Brian D. McCabe, 2022. "Retromer deficiency in Tauopathy models enhances the truncation and toxicity of Tau," Nature Communications, Nature, vol. 13(1), pages 1-16, December.

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