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Postsynaptic synaptotagmins mediate AMPA receptor exocytosis during LTP
Dick Wu1,2,3, Taulant Bacaj1, Wade Morishita2,3
1Department of Molecular &Cellular Physiology and Howard Hughes Medical Institute, Stanford University Medical School, Stanford, California 94305, USA.
Nature
|March 30, 2017
Summary
Synaptotagmin-1 and synaptotagmin-7 act as redundant calcium sensors to facilitate AMPA receptor exocytosis during long-term potentiation (LTP), a key process for learning and memory.
Area of Science:
- Neuroscience
- Molecular Biology
Background:
- Long-term potentiation (LTP) strengthens synaptic connections, mediated by NMDA receptor activation and subsequent calcium influx.
- Calcium influx during LTP induction stimulates the recruitment of synaptic AMPA receptors, but the underlying mechanism remains unclear.
Purpose of the Study:
- To elucidate the role of synaptotagmins in calcium-dependent AMPA receptor recruitment during LTP.
Main Methods:
- Investigated the effects of blocking postsynaptic synaptotagmin-1 (Syt1) and synaptotagmin-7 (Syt7) expression on LTP in mouse hippocampal CA1 pyramidal neurons.
- Utilized wild-type and Ca2+-binding-deficient Syt7 mutants, as well as dominant-negative Syt1 mutants, to assess protein function.
Main Results:
- Simultaneous blockade of postsynaptic Syt1 and Syt7 abolished LTP, while blocking either alone did not.
- LTP was restored by wild-type Syt7 but not a Ca2+-binding-deficient mutant, indicating a requirement for calcium binding.
- Expression of a dominant-negative Syt1 mutant inhibited Ca2+-dependent postsynaptic AMPA receptor exocytosis and blocked LTP.
Conclusions:
- Postsynaptic Syt1 and Syt7 function redundantly as calcium sensors for the exocytosis of AMPA receptors during LTP.
- This identifies a novel mechanism for AMPA receptor recruitment essential for synaptic plasticity, learning, and memory.
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