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Astrocytic EphB3 receptors regulate d-serine-gated synaptic plasticity and memory.

Valentin Clément Langlais¹, Sarah Mountadem¹, Ines Benazzouz¹

¹Univ. Bordeaux, INSERM, Neurocentre Magendie, U1215, Bordeaux F-33000, France.

Progress in Neurobiology

|March 13, 2025

Summary

Astrocytes regulate brain function via EphB3 receptors, controlling NMDA receptor (NMDAR) activity, synaptic plasticity, and memory. This study highlights astrocyte-neuron interactions crucial for learning and memory.

Keywords:

Astrocyte D-serine Ephrin LTP Memory NMDA receptor

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Area of Science:

Neuroscience
Cell Biology
Synaptic Plasticity

Background:

NMDA receptors (NMDARs) require co-agonists like d-serine for activation.
The precise mechanisms of astrocyte-neuron communication regulating synaptic d-serine remain unclear.
Cell adhesion molecules are implicated in astrocytic and neuronal interactions at synapses.

Purpose of the Study:

To investigate the role of astrocytic EphB3 receptors and their neuronal partner, ephrinB3, in regulating synaptic function.
To determine the impact of EphB3 signaling on NMDAR activity, synaptic plasticity, and memory.

Main Methods:

Acute hippocampal slice electrophysiology in adult mice.
Stimulation and inhibition of EphB3 receptors.
Knockdown of astrocytic EphB3 receptors.
Novel object recognition memory tests.

Main Results:

EphB3 receptor stimulation increased synaptic d-serine availability and NMDAR activity.
Inhibition of EphB3 receptors impaired NMDAR activity and LTP, rescued by d-serine.
Astrocytic EphB3 knockdown mimicked these impairments and caused memory deficits.

Conclusions:

Astrocytic EphB3 receptors are critical for synaptic NMDAR function in the hippocampus.
EphB3 signaling in astrocytes regulates activity-dependent synaptic plasticity and memory formation.
This study elucidates a novel mechanism of astrocyte-neuron communication essential for cognitive processes.