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SAP102 regulates synaptic AMPAR function through a CNIH-2-dependent mechanism.

Mingna Liu^1,2, Rebecca Shi^1,2,3, Hongik Hwang^1,4

¹Picower Institute for Learning and Memory, Massachusetts Institute of Technology , Cambridge, Massachusetts.

Journal of Neurophysiology

|August 2, 2018

Summary

SAP102 protein rescues synaptic function by restoring alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) currents after PSD-95 knockdown. SAP102 uniquely increases AMPAR current decay time, requiring cornichon-2, unlike PSD-95.

Keywords:

DLG-MAGUK PSD-MAGUK excitatory synapse hippocampus slice culture

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Area of Science:

Neuroscience
Molecular Biology
Cell Biology

Background:

Postsynaptic density (PSD)-95-like, disk-large (DLG) membrane-associated guanylate kinase (PSD/DLG-MAGUK) proteins scaffold alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) complexes.
These PSD/DLG-MAGUKs are crucial for activity-dependent modulation of synaptic AMPAR functions.
SAP102 is a key PSD/DLG-MAGUK member present throughout life, playing a significant role in synaptic development and function.

Purpose of the Study:

To investigate the specific role of SAP102 in synaptic transmission.
To determine how SAP102 influences AMPAR function in the context of PSD-95 knockdown.
To elucidate the differential contributions of SAP102 and PSD-95 to synaptic properties and kinetics.

Main Methods:

Utilized a cell-restricted molecular replacement strategy to express SAP102 against a background of acute PSD-95 knockdown.
Measured AMPAR-mediated evoked excitatory postsynaptic currents (eEPSCs) and miniature EPSCs (mEPSCs).
Analyzed the impact of SAP102 and PSD-95 on AMPAR mEPSC decay time and the requirement of cornichon-2.

Main Results:

SAP102 successfully rescued the decrease in AMPAR eEPSCs and mEPSC frequency caused by PSD-95 knockdown.
Replacement of PSD-95 with SAP102, but not direct PSD-95 manipulation, increased AMPAR mEPSC decay time.
SAP102-mediated rescue of AMPAR eEPSCs was dependent on the AMPAR auxiliary subunit cornichon-2, unlike PSD-95's regulation.

Conclusions:

SAP102 and PSD-95 differentially regulate basic synaptic properties and synaptic current kinetics.
SAP102 influences AMPAR function, specifically mEPSC decay time, in a manner distinct from PSD-95.
The distinct effects of SAP102 and PSD-95 may involve interactions with different AMPAR auxiliary subunits, such as cornichon-2, leading to specific modulation of excitatory circuits.