Projects per year
Membrane trafficking of AMPA receptors (AMPARs) is critical for neuronal function and plasticity. Although rapid forms of AMPAR internalization during long-term depression (LTD) require clathrin and dynamin, the mechanisms governing constitutive AMPAR turnover and internalization of AMPARs during slow homeostatic forms of synaptic plasticity remain unexplored. Here, we show that, in contrast to LTD, constitutive AMPAR internalization and homeostatic AMPAR downscaling in rat neurons do not require dynamin or clathrin function. Instead, constitutive AMPAR trafficking is blocked by a Rac1 inhibitor and is regulated by a dynamic nonstructural pool of F-actin. Our findings reveal a novel role for neuronal clathrin-independent endocytosis controlled by actin dynamics and suggest that the interplay between different modes of receptor endocytosis provides for segregation between distinct modes of neuronal plasticity.
Bibliographical noteCopyright © 2015 Glebov et al.
- Cell Culture Techniques
- Long-Term Synaptic Depression
- Protein Transport
- RNA, Small Interfering
- Receptors, AMPA
- rac1 GTP-Binding Protein
Roles of protein SUMOylation in AMPA receptor trafficking, synaptic dysfunction and cognitive impairment in dementia
1/03/14 → 30/06/18
Regulation of spine Ca2+ dynamics and spike timing-dependent synaptic plasticity by muscarinic acetylcholine receptors
1/10/12 → 1/10/15