| First Author | Steinmetz CC | Year | 2016 |
| Journal | Cell Rep | Volume | 16 |
| Issue | 10 | Pages | 2711-2722 |
| PubMed ID | 27568566 | Mgi Jnum | J:239017 |
| Mgi Id | MGI:5824779 | Doi | 10.1016/j.celrep.2016.08.009 |
| Citation | Steinmetz CC, et al. (2016) Upregulation of mu3A Drives Homeostatic Plasticity by Rerouting AMPAR into the Recycling Endosomal Pathway. Cell Rep 16(10):2711-22 |
| abstractText | Synaptic scaling is a form of homeostatic plasticity driven by transcription-dependent changes in AMPA-type glutamate receptor (AMPAR) trafficking. To uncover the pathways involved, we performed a cell-type-specific screen for transcripts persistently altered during scaling, which identified the mu subunit (mu3A) of the adaptor protein complex AP-3A. Synaptic scaling increased mu3A (but not other AP-3 subunits) in pyramidal neurons and redistributed dendritic mu3A and AMPAR to recycling endosomes (REs). Knockdown of mu3A prevented synaptic scaling and this redistribution, while overexpression (OE) of full-length mu3A or a truncated mu3A that cannot interact with the AP-3A complex was sufficient to drive AMPAR to REs. Finally, OE of mu3A acted synergistically with GRIP1 to recruit AMPAR to the dendritic membrane. These data suggest that excess mu3A acts independently of the AP-3A complex to reroute AMPAR to RE, generating a reservoir of receptors essential for the regulated recruitment to the synaptic membrane during scaling up. |
