High-resolution imaging and manipulation of endogenous AMPA receptor surface mobility during synaptic plasticity and learning
Autor: | Sophie Daburon, Agata Nowacka, Eric Hosy, Mathieu Ducros, Hanna L. Zieger, Matthieu Sainlos, Daniel Choquet, Mónica Fernández-Monreal, Angela M. Getz, Urielle François, Christelle Breillat, Frederic Lanore, Aurélie Lampin-Saint-Amaux, Yann Humeau |
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Přispěvatelé: | Interdisciplinary Institute for Neuroscience [Bordeaux] (IINS), Université de Bordeaux (UB)-Centre National de la Recherche Scientifique (CNRS) |
Rok vydání: | 2022 |
Předmět: |
Lattice Light Sheet Microscopy
Biotin AMPA receptor BirA AMPA Receptor 03 medical and health sciences Learning and Memory 0302 clinical medicine Neurotransmitter receptor Receptor 030304 developmental biology 0303 health sciences Multidisciplinary biology Chemistry NeutrAvidin Glutamate receptor Long-term potentiation Lateral surface diffusion GluA2 Biotinylation Synaptic plasticity biology.protein monomeric StreptAvidin [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC] Neuroscience 030217 neurology & neurosurgery Synaptic Plasticity Avidin |
Zdroj: | Science advances. 8(30) |
ISSN: | 2375-2548 |
Popis: | SUMMARYRegulation of synaptic neurotransmitter receptor content is a fundamental mechanism for tuning synaptic efficacy during experience-dependent plasticity and behavioral adaptation. However, experimental approaches to track and modify receptor movements in integrated experimental systems are limited. Exploiting AMPA-type glutamate receptors (AMPAR) as a model, we generated a knock-in mouse expressing the biotin acceptor peptide (AP) tag on the GluA2 extracellular N-terminus. Cell-specific introduction of biotin ligase allows the use of monovalent or tetravalent avidin variants to respectively monitor or manipulate the surface mobility of endogenous AMPAR containing biotinylated AP-GluA2 in neuronal subsets. AMPAR immobilization precluded the expression of long-term potentiation and formation of contextual fear memory, allowing for target-specific control of the expression of synaptic plasticity and animal behavior. The AP tag knock-in model offers unprecedented access to resolve and control the spatiotemporal dynamics of endogenous receptors, and opens new avenues to study the molecular mechanisms of synaptic plasticity and learning. |
Databáze: | OpenAIRE |
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