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Updated: Dec 1, 2025

A High-throughput Calcium-flux Assay to Study NMDA-receptors with Sensitivity to Glycine/D-serine and Glutamate
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Postsynaptic Serine Racemase Regulates NMDA Receptor Function.

Jonathan M Wong1,2, Oluwarotimi O Folorunso3,4, Eden V Barragan1,2

  • 1Center for Neuroscience, University of California Davis, Davis, California 95616.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|November 7, 2020
PubMed
Summary
This summary is machine-generated.

Serine racemase (SR) synthesizes d-serine, crucial for NMDAR function. This study reveals SR’s postsynaptic role in neurons, impacting synaptic plasticity and NMDAR regulation.

Keywords:
GluN2ANR2ANR2BSrrglycineplasticity

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Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Molecular Biology

Background:

  • d-serine is a key NMDAR coagonist in the forebrain.
  • Serine racemase (SR) synthesizes d-serine, but its precise localization and function remain debated.
  • Previous research suggested astrocytic but recent findings point to neuronal SR, potentially at the postsynaptic density.

Purpose of the Study:

  • To investigate the localization and function of serine racemase (SR) and d-serine in mature forebrain synapses.
  • To determine the cell-autonomous role of SR in regulating NMDAR function and synaptic plasticity.
  • To explore the implications of postsynaptic SR on synaptic transmission and potential autocrine signaling.

Main Methods:

  • Immunohistochemistry and electron microscopy in mouse CA1 pyramidal neurons to visualize SR and d-serine localization.
  • Single-neuron genetic deletion of SR in conditional knockout mice (both sexes).
  • Electrophysiological recordings to assess NMDAR function and long-term potentiation (LTP) at Schaffer collateral (CA3)-CA1 synapses.

Main Results:

  • Age-dependent dendritic and postsynaptic localization of SR and d-serine was observed.
  • Single-neuron genetic deletion of SR impaired LTP, which was rescued by exogenous d-serine.
  • LTP was restored by 2 months of age, correlating with increased synaptic GluN2B, suggesting compensatory mechanisms.

Conclusions:

  • Postsynaptic neuronal SR plays a cell-autonomous role in regulating synaptic NMDAR function.
  • These findings support a model where d-serine acts in an autocrine manner at synapses.
  • The study elucidates a novel mechanism for regulating synaptic plasticity via postsynaptic d-serine synthesis.