Metabotropic glutamate receptor

Spillover effect

NMDA receptor

Neuroscience

Biology

Excitatory postsynaptic potential

Microeconomics

Receptor

Inhibitory postsynaptic potential

Economics

Neurotransmission

Biochemistry

LTP induction

Actin cytoskeleton

Psychology

Glutamate receptor

Cytoskeleton

Cofilin

Chemistry

Cell

Long-term potentiation

Synapse

Neuron

Extrasynaptic actions of glutamate are limited by high-affinity transporters expressed by perisynaptic astroglial processes (PAPs): this helps maintain point-to-point transmission in excitatory circuits. Memory formation in the brain is associated with synaptic remodeling, but how this affects PAPs and therefore extrasynaptic glutamate actions is poorly understood. Here, we used advanced imaging methods, in situ and in vivo, to find that a classical synaptic memory mechanism, long-term potentiation (LTP), triggers withdrawal of PAPs from potentiated synapses. Optical glutamate sensors combined with patch-clamp and 3D molecular localization reveal that LTP induction thus prompts spatial retreat of astroglial glutamate transporters, boosting glutamate spillover and NMDA-receptor-mediated inter-synaptic cross-talk. The LTP-triggered PAP withdrawal involves NKCC1 transporters and the actin-controlling protein cofilin but does not depend on major Ca

LTP Induction Boosts Glutamate Spillover by Driving Withdrawal of Perisynaptic Astroglia