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Doc2-mediated superpriming supports synaptic augmentation.

Renhao Xue1,2, David A Ruhl1,2,3, Joseph S Briguglio1,2

  • 1Howard Hughes Medical Institute, University of Wisconsin-Madison, Madison, WI 53705-2275.

Proceedings of the National Academy of Sciences of the United States of America
|May 31, 2018
PubMed
Summary
This summary is machine-generated.

Doc2, a calcium sensor, drives synaptic augmentation, a short-term plasticity form crucial for learning and memory. Its absence impairs this process by affecting vesicle priming, distinct from other plasticity mechanisms.

Keywords:
Doc2munc13short-term plasticitysuperprimingsynaptic augmentation

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cellular Physiology

Background:

  • Synaptic plasticity, including short-term enhancement like augmentation, is fundamental to learning and memory.
  • The precise molecular mechanisms governing synaptic augmentation remain incompletely understood, with residual presynaptic calcium (Ca2+) implicated.

Purpose of the Study:

  • To investigate the role of the calcium sensor Doc2 in synaptic augmentation.
  • To elucidate the molecular mechanisms by which Doc2 mediates short-term synaptic plasticity.

Main Methods:

  • Utilized cultured mouse hippocampal neurons, including Doc2-deficient models.
  • Assessed synaptic augmentation and other forms of short-term enhancement.
  • Investigated changes in readily releasable pool size, Ca2+ dynamics, and vesicle priming.

Main Results:

  • Synaptic augmentation was significantly reduced in neurons lacking Doc2, while other short-term enhancements remained unaffected.
  • Doc2 binds Ca2+ and munc13, translocating to the plasma membrane to facilitate augmentation.
  • The mechanism involved superpriming of synaptic vesicles, independent of altered readily releasable pool size or Ca2+ dynamics.

Conclusions:

  • Doc2 acts as a crucial Ca2+ sensor for synaptic augmentation.
  • Doc2 mediates synaptic augmentation through a mechanism involving vesicle superpriming, distinct from other plasticity forms.
  • These findings identify Doc2 as a key component of the Ca2+-sensing machinery in short-term synaptic plasticity.