Journal
CELL REPORTS
Volume 19, Issue 12, Pages 2613-2626Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2017.06.001
Keywords
-
Categories
Funding
- MRC [MR/L003791]
- Wellcome Trust [102388/Z/13/Z, 105384/Z/14/Z]
- BHF [PG/14/60/31014]
- BBSRC [BB/K014366, BB/K014358]
- Wellcome Trust [102388/Z/13/Z, 105384/Z/14/Z] Funding Source: Wellcome Trust
- BBSRC [BB/K014358/1, BB/F00723X/1] Funding Source: UKRI
- MRC [MR/L003791/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/F00723X/1, BB/K014358/1] Funding Source: researchfish
- British Heart Foundation [PG/14/60/31014] Funding Source: researchfish
- Medical Research Council [G0601810, MR/L003791/1] Funding Source: researchfish
Ask authors/readers for more resources
Ionotropic glutamate receptor (iGluR) trafficking and function underpin excitatory synaptic transmission and plasticity and shape neuronal networks. It is well established that the transcription, translation, and endocytosis/recycling of iGluRs are all regulated by neuronal activity, but much less is known about the activity dependence of iGluR transport through the secretory pathway. Here, we use the kainate receptor subunit GluK2 as a model iGluR cargo to show that the assembly, early secretory pathway trafficking, and surface delivery of iGluRs are all controlled by neuronal activity. We show that the delivery of de novo kainate receptors is differentially regulated by modulation of GluK2 Q/R editing, PKC phosphorylation, and PDZ ligand interactions. These findings reveal that, in addition to short-term regulation of iGluRs by recycling/endocytosis and long-term modulation by altered transcription/translation, the trafficking of iGluRs through the secretory pathway is under tight activity-dependent control to determine the numbers and properties of surface-expressed iGluRs.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available