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Differential Effect on Hippocampal Synaptic Facilitation by the Presynaptic Protein Mover
Julio S Viotti1, Thomas Dresbach1
1Institute of Anatomy and Embryology, University Medical Center Göttingen, Georg-August University of Göttingen, Göttingen, Germany.
Frontiers in Synaptic Neuroscience
|December 6, 2019
Summary
The presynaptic protein Mover normally limits synaptic facilitation at specific brain synapses. Its absence in knockout mice leads to increased, calcium- and age-dependent facilitation, particularly in mossy fiber terminals.
Area of Science:
- Neuroscience
- Molecular Biology
- Synaptic Plasticity
Background:
- Neurotransmitter release is mediated by a conserved presynaptic machinery.
- Some presynaptic proteins are variably expressed, suggesting modulatory roles.
- The specific functions of Mover/TPRGL/SVAP30, a heterogeneously expressed presynaptic protein, remain unclear.
Purpose of the Study:
- To investigate the role of the presynaptic protein Mover in synaptic function.
- To determine how Mover influences neurotransmitter release at different synapse types.
Main Methods:
- Utilized a Mover knockout mouse line.
- Examined synaptic function at hippocampal mossy fiber (MF) to CA3 and Schaffer collateral to CA1 synapses.
- Assessed the impact of calcium concentration and animal age on synaptic facilitation.
- Investigated the effect of forskolin-induced cyclic adenosine monophosphate (cAMP) potentiation.
Main Results:
- Mover knockout did not alter Schaffer collateral synapses.
- Mover knockout significantly increased facilitation at MF synapses.
- The increased facilitation in Mover knockout mice was calcium- and age-dependent.
- Forskolin equally potentiated both wildtype and knockout MF synapses, but occluded the knockout-induced facilitation.
Conclusions:
- Mover plays a synapse-specific role in regulating presynaptic function.
- At MF terminals, Mover acts to constrain the degree of presynaptic facilitation.
- Mover's function is modulated by calcium levels and animal age.
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