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Selective molecular impairment of spontaneous neurotransmission modulates synaptic efficacy

Author

Listed:
  • Devon C. Crawford

    (UT Southwestern Medical Center)

  • Denise M. O. Ramirez

    (Whole Brain Microscopy Facility, UT Southwestern Medical Center)

  • Brent Trauterman

    (UT Southwestern Medical Center)

  • Lisa M. Monteggia

    (UT Southwestern Medical Center)

  • Ege T. Kavalali

    (UT Southwestern Medical Center
    UT Southwestern Medical Center)

Abstract

Recent studies suggest that stimulus-evoked and spontaneous neurotransmitter release processes are mechanistically distinct. Here we targeted the non-canonical synaptic vesicle SNAREs Vps10p-tail-interactor-1a (vti1a) and vesicle-associated membrane protein 7 (VAMP7) to specifically inhibit spontaneous release events and probe whether these events signal independently of evoked release to the postsynaptic neuron. We found that loss of vti1a and VAMP7 impairs spontaneous high-frequency glutamate release and augments unitary event amplitudes by reducing postsynaptic eukaryotic elongation factor 2 kinase (eEF2K) activity subsequent to the reduction in N-methyl-D-aspartate receptor (NMDAR) activity. Presynaptic, but not postsynaptic, loss of vti1a and VAMP7 occludes NMDAR antagonist-induced synaptic potentiation in an intact circuit, confirming the role of these vesicular SNAREs in setting synaptic strength. Collectively, these results demonstrate that spontaneous neurotransmission signals independently of stimulus-evoked release and highlight its role as a key regulator of postsynaptic efficacy.

Suggested Citation

  • Devon C. Crawford & Denise M. O. Ramirez & Brent Trauterman & Lisa M. Monteggia & Ege T. Kavalali, 2017. "Selective molecular impairment of spontaneous neurotransmission modulates synaptic efficacy," Nature Communications, Nature, vol. 8(1), pages 1-14, April.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms14436
    DOI: 10.1038/ncomms14436
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    Cited by:

    1. Radhika Rawat & Elif Tunc-Ozcan & Tammy L. McGuire & Chian-Yu Peng & John A. Kessler, 2022. "Ketamine activates adult-born immature granule neurons to rapidly alleviate depression-like behaviors in mice," Nature Communications, Nature, vol. 13(1), pages 1-12, December.

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