| First Author | Getz AM | Year | 2022 |
| Journal | Sci Adv | Volume | 8 |
| Issue | 30 | Pages | eabm5298 |
| PubMed ID | 35895810 | Mgi Jnum | J:330791 |
| Mgi Id | MGI:7329501 | Doi | 10.1126/sciadv.abm5298 |
| Citation | Getz AM, et al. (2022) High-resolution imaging and manipulation of endogenous AMPA receptor surface mobility during synaptic plasticity and learning. Sci Adv 8(30):eabm5298 |
| abstractText | Regulation 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 (AMPARs) as a model, we generated a knock-in mouse expressing the biotin acceptor peptide (AP) tag on the GluA2 extracellular N-terminal. 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 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. |
