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Related Experiment Video

Updated: Jul 2, 2026

A High-throughput Calcium-flux Assay to Study NMDA-receptors with Sensitivity to Glycine/D-serine and Glutamate

A High-throughput Calcium-flux Assay to Study NMDA-receptors with Sensitivity to Glycine/D-serine and Glutamate

Published on: July 10, 2018

Neuronal viability is controlled by a functional relation between synaptic and extrasynaptic NMDA receptors.

F Léveillé¹, F El Gaamouch, E Gouix

¹UMR 6232 Centre National de la Recherche Scientifique-Université de Caen, GIP CYCERON, Bd Henri Becquerel, BP 5229 14074 Caen, France.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology

|August 20, 2008

Summary

Targeting extrasynaptic N-methyl-D-aspartate receptors (NMDARs) offers a promising therapeutic strategy for brain injuries. Selective activation of extrasynaptic NMDARs causes neuronal damage, unlike synaptic NMDARs.

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Published on: July 10, 2018

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Microtransplantation of Synaptic Membranes to Reactivate Human Synaptic Receptors for Functional Studies

Microtransplantation of Synaptic Membranes to Reactivate Human Synaptic Receptors for Functional Studies

Published on: July 20, 2022

Area of Science:

Neuroscience
Cell Biology
Pharmacology

Background:

N-methyl-D-aspartate receptors (NMDARs) are crucial for learning and memory but implicated in neuronal damage.
The cellular location (synaptic vs. extrasynaptic) of NMDARs influences neuronal viability.

Purpose of the Study:

To investigate the relationship between synaptic and extrasynaptic NMDAR pools.
To determine the role of these NMDAR pools in beneficial and detrimental neuronal events.

Main Methods:

Selective activation of extrasynaptic NMDARs.
Assessment of extracellular signal-regulated kinase (ERK) pathway activation.
Measurement of mitochondrial membrane potential.
Evaluation of cellular damage (cell body and dendrites).
Analysis of NMDAR antagonist memantine's effects.

Main Results:

Extrasynaptic NMDAR activation, unlike synaptic NMDAR activation, did not activate ERK pathways.
Extrasynaptic NMDAR activation led to mitochondrial dysfunction and cellular damage.
Synaptic NMDAR activation was innocuous and induced sustained ERK activation.
Glutamate uptake systems control the functional difference between NMDAR pools.
Memantine preferentially antagonizes extrasynaptic NMDARs.

Conclusions:

Extrasynaptic NMDAR activation contributes to excitotoxicity.
Targeting extrasynaptic NMDARs is a potential therapeutic strategy for brain injuries.
Functional dichotomy between NMDAR pools is regulated by glutamate uptake.