scholarly journals Biophysical Model of AMPA Receptor Trafficking and Its Regulation during Long-Term Potentiation/Long-Term Depression

2006 ◽  
Vol 26 (47) ◽  
pp. 12362-12373 ◽  
Author(s):  
B. A. Earnshaw ◽  
P. C. Bressloff
Keyword(s):  
Ampa Receptor ◽  
Long Term Potentiation ◽  
Receptor Trafficking ◽  
Biophysical Model ◽  
Long Term Depression ◽  
Term Potentiation ◽  
Ampa Receptor Trafficking

scholarly journals AMPA receptor trafficking and long-term potentiation

2003 ◽  
Vol 358 (1432) ◽  
pp. 707-714 ◽  
Author(s):  
Roberto Malinow
Keyword(s):  
Ampa Receptor ◽  
Critical Role ◽  
Long Term Potentiation ◽  
Receptor Trafficking ◽  
Synaptic Function ◽  
Term Potentiation ◽  
The Subject ◽  
Activity Dependent ◽  
Ampa Receptor Trafficking

Activity-dependent changes in synaptic function are believed to underlie the formation of memories. A prominent example is long-term potentiation (LTP), whose mechanisms have been the subject of considerable scrutiny over the past few decades. I review studies from our laboratory that support a critical role for AMPA receptor trafficking in LTP and experience-dependent plasticity.

scholarly journals Synaptic activity regulates AMPA receptor trafficking through different recycling pathways

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Ning Zheng ◽  
Okunola Jeyifous ◽  
Charlotte Munro ◽  
Johanna M Montgomery ◽  
William N Green
Keyword(s):  
Long Term Potentiation ◽  
Receptor Trafficking ◽  
Synaptic Activity ◽  
Transferrin Receptors ◽  
Long Term Depression ◽  
Recycling Endosomes ◽  
Surface Receptors ◽  
Term Potentiation ◽  
Dependent Pathway

Changes in glutamatergic synaptic strength in brain are dependent on AMPA-type glutamate receptor (AMPAR) recycling, which is assumed to occur through a single local pathway. In this study, we present evidence that AMPAR recycling occurs through different pathways regulated by synaptic activity. Without synaptic stimulation, most AMPARs recycled in dynamin-independent endosomes containing the GTPase, Arf6. Few AMPARs recycled in dynamin-dependent endosomes labeled by transferrin receptors (TfRs). AMPAR recycling was blocked by alterations in the GTPase, TC10, which co-localized with Arf6 endosomes. TC10 mutants that reduced AMPAR recycling had no effect on increased AMPAR levels with long-term potentiation (LTP) and little effect on decreased AMPAR levels with long-term depression. However, internalized AMPAR levels in TfR-containing recycling endosomes increased after LTP, indicating increased AMPAR recycling through the dynamin-dependent pathway with synaptic plasticity. LTP-induced AMPAR endocytosis is inconsistent with local recycling as a source of increased surface receptors, suggesting AMPARs are trafficked from other sites.

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