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Published on: July 15, 2012
Synapsins regulate use-dependent synaptic plasticity in the calyx of Held by a Ca2+/calmodulin-dependent pathway
Jianyuan Sun1, Peter Bronk, Xinran Liu
1Center for Basic Neuroscience, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, TX 75390-9111, USA. jianyuan.sun@utsouthwestern.edu
Summary
Synapsins (SYN) do not affect basic neurotransmitter release but enhance release probability during high-frequency stimulation. This function involves calcium/calmodulin-dependent processes, crucial for synaptic plasticity.
Area of Science:
- Neuroscience
- Cell Biology
- Molecular Biology
Background:
- Synapsins are key synaptic vesicle phosphoproteins regulating neurotransmitter release.
- Their precise role, especially during high-frequency activity, remains incompletely understood.
Purpose of the Study:
- To investigate the function of synapsins 1 and 2 in neurotransmitter release at the calyx of Held synapse.
- To elucidate the mechanisms underlying synapsin-mediated regulation of synaptic transmission.
Main Methods:
- Utilized synapsin 1 and 2 knockout mice for functional analysis of the calyx of Held synapse.
- Performed precise measurements of neurotransmitter release under various stimulation conditions.
Main Results:
- Synapsin deletion did not alter spontaneous release, action potential-evoked release, readily releasable pool (RRP) size, or RRP recovery kinetics.
- Deletion of synapsins significantly increased use-dependent synaptic depression during high-frequency stimulation (>50 Hz).
- This increased depression resulted from a reduced fraction of RRP release evoked by later action potentials in a train.
Conclusions:
- Synapsins enhance release probability during high-frequency stimulation, suggesting a role in synaptic plasticity.
- The observed effect is likely mediated by Ca2+/calmodulin-dependent phosphorylation of synapsins, modulating vesicle release dynamics.
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