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Arc/Arg3.1 function in long-term synaptic plasticity: Emerging mechanisms and unresolved issues
Hongyu Zhang1, Clive R Bramham1
1Department of Biomedicine, University of Bergen, Bergen, Norway.
The European Journal of Neuroscience
|September 5, 2020
Summary
Activity-regulated cytoskeleton-associated protein (Arc) bidirectionally controls synaptic strength by regulating AMPA-type glutamate receptor trafficking and actin dynamics. This protein is crucial for memory and brain development.
Area of Science:
- Neuroscience
- Molecular Biology
- Synaptic Plasticity
Background:
- Activity-regulated cytoskeleton-associated protein (Arc) plays a key role in synaptic plasticity and memory.
- The precise mechanisms by which Arc bidirectionally regulates synaptic strength remain unclear.
Purpose of the Study:
- To review evidence on Arc function in various plasticity paradigms.
- To propose a model for Arc's role in bidirectionally controlling synaptic strength.
- To highlight outstanding questions and stimulus-specific mechanisms of Arc function.
Main Methods:
- Literature review of plasticity paradigms.
- Analysis of existing data on Arc function.
- Model proposal based on current evidence.
Main Results:
- Arc is implicated in multiple forms of synaptic plasticity, including LTP and LTD.
- Arc's function is stimulus-dependent and dictates synaptic strength.
- A model is proposed where Arc coordinates AMPAR trafficking and actin dynamics.
Conclusions:
- Arc bidirectionally controls synaptic strength through coordinated regulation of AMPA-type glutamate receptor (AMPAR) trafficking and actin cytoskeletal dynamics.
- Arc acts as an activity-dependent regulator of AMPAR lateral diffusion and synaptic trapping.
- Understanding Arc's mechanisms is vital for comprehending memory formation and cortical development.
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