Team Choquet and collaborators in Neuron
When synapses adjust information transfer thanks to mobile receptors
How does the brain treat rapid signals without overloading? That’s the question asked by CNRS and University of Bordeaux’s researchers in their study published in Neuron on February 4th 2026, in a collaboration with scientists at the Bordeaux Imaging Center, at Ottawa university, at Sussex Neuroscience and at the Vrije Universiteit Amsterdam.
They show that AMPA receptor’s mobility on neurons’ surface plays a key role in filtration and amplification of information. By moving through synapses, those receptors allow to maintain the transmission during rapid stimulations. This mechanism, variable depending on the synapses, links plasticity, neural calculation and learning.
All synapses do not transfer information in the same way. Some amplify rapid signals and others diminish them. This phenomenon is called short-term synaptic plasticity and is essential for information treatment in the brain. Until now, it was mainly attributed to the regulation of release of pre-synaptic neurotransmitters.
This study spotlights a complementary mechanism located on the post-synaptic side: AMPA receptors’ mobility.
Thanks to a line of genetically modified mice developed in the Choquet lab, researchers followed the movement of these receptors in real time and controlled their ability to move on neurons’ surface. Combining advanced imaging, optical captors of synaptic activity and electrophysiological experiments, they could observe that this mobility plays a key role when synapses are highly stimulated.
In standard situation, AMPA receptors can desensitize themselves temporarily after a repeated activity. Their mobility allows “new” receptors to replace the inefficient ones, maintaining the transmission of the signal. When this movement is blocked, desensitized receptors stay trapped in the synapse. The transmission highly diminishes and the synapse acts as a brake.
Therefore, this mechanism acts like a speeding and a slowdown system integrated in each synapse. The researchers observed that all synapses did not act in the same way. Depending on the architecture and molecular properties of the synapses, some were more sensitive to receptors mobility than others. Each synapse seems to have its own “dynamic signature” for treating information.
Researchers also found that the forms of synaptic plasticity associated with learning modify this mobility, linking directly memory mechanisms to the way synapses treat instant signals.
These results open up new paths. Many physiological or pathological factors – such as stress, aging, neurodegenerative diseases – influence AMPA receptors mobility. This could be of great interest to modulate neural networks functioning.
Figure: On the left, a synaptic spine. Inactive AMPA receptors (grey) spread on the surface of the synapse (1) and are reversibly accumulated where the neurotransmitter, glutamate, is released. Receptors are activated by glutamate which is released by the presynaptic terminal (3), then desensitize (2). The exchange by diffusion of these desensitized receptors allows their replacement by new activatable receptors. Therefore, AMPA receptors’ mobility contributes to recovery from synaptic depression during repeated stimulation.
On the right, a Shapley diagram, coming from the game theory, helps estimate the respective contributions of receptors’ mobility (1), their desensitization (2) and the potential glutamate release (3) on the evolution of short-term synaptic plasticity.
For more information
Synapse-specific and plasticity-regulated AMPA receptor mobility tunes synaptic integration, Agata Nowacka, Angela M. Getz, Hanna L. Zieger, Maxime Malivert, Diogo Bessa-Neto, Elisabete Augusto, Christelle Breillat, Sophie Daburon, Cécile Lemoigne, Sébastien Marais, Mathieu Ducros, Alexandre Favereaux, Andrew C. Penn, Richard Naud, Matthieu Sainlos, Daniel Choquet.
Neuron, February 4th 2026.
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GPR director – Team leader – BIC Director