PMID- 23460828
OWN - NLM
STAT- MEDLINE
DCOM- 20130903
LR  - 20211021
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 8
IP  - 2
DP  - 2013
TI  - Acute BDNF treatment upregulates GluR1-SAP97 and GluR2-GRIP1 interactions: 
      implications for sustained AMPA receptor expression.
PG  - e57124
LID - 10.1371/journal.pone.0057124 [doi]
LID - e57124
AB  - Brain-derived neurotrophic factor (BDNF) plays several prominent roles in 
      synaptic plasticity and in learning and memory formation. Reduced BDNF levels and 
      altered BDNF signaling have been reported in several brain diseases and 
      behavioral disorders, which also exhibit reduced levels of AMPAr subunits. BDNF 
      treatment acutely regulates AMPA receptor expression and function, including 
      synaptic AMPAr subunit trafficking, and implicates several well defined signaling 
      molecules that are required to elicit long term potentiation and depression (LTP 
      and LTD, respectively). Long term encoding of synaptic events, as in long term 
      memory formation, requires AMPAr stabilization and maintenance. However, factors 
      regulating AMPAr stabilization in neuronal cell membranes and synaptic sites are 
      not well characterized. In this study, we examine the effects of acute BDNF 
      treatment on levels of AMPAr-associated scaffolding proteins and on AMPAr 
      subunit-scaffolding protein interactions. We also examine the effects of 
      BDNF-dependent enhanced interactions between AMPAr subunits with their specific 
      scaffolding proteins on the accumulation of both types of proteins. Our results 
      show that acute BDNF treatment upregulates the interactions between AMPAr 
      subunits (GluR1 and GluR2) with their scaffold proteins SAP97 and GRIP1, 
      respectively, leading to prolonged increased accumulation of both categories of 
      proteins, albeit with distinct mechanisms for GluR1 and GluR2. Our findings 
      reveal a new role for BDNF in the long term maintenance of AMPA receptor subunits 
      and associated scaffolding proteins at synapses and further support the role of 
      BDNF as a key regulator of synaptic consolidation. These results have potential 
      implications for recent findings implicating BDNF and AMPAr subunits in various 
      brain diseases and behavioral disorders.
FAU - Jourdi, Hussam
AU  - Jourdi H
AD  - Department of Biomedical Sciences, College of Medicine, Florida State University, 
      Tallahassee, Florida, United States of America. hjourdi@fsu.edu
FAU - Kabbaj, Mohamed
AU  - Kabbaj M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130227
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Carrier Proteins)
RN  - 0 (Dlg1 protein, rat)
RN  - 0 (Grip1 protein, rat)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (Membrane Proteins)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Receptors, AMPA)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - P6W5IXV8V9 (glutamate receptor ionotropic, AMPA 2)
RN  - TFZ3H25BS1 (glutamate receptor ionotropic, AMPA 1)
SB  - IM
MH  - Adaptor Proteins, Signal Transducing/*metabolism
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*pharmacology
MH  - Carrier Proteins/*metabolism
MH  - Cell Membrane/drug effects/metabolism
MH  - Cells, Cultured
MH  - Cerebral Cortex/cytology
MH  - Gene Knockdown Techniques
MH  - HEK293 Cells
MH  - Humans
MH  - Intracellular Signaling Peptides and Proteins
MH  - Membrane Proteins/*metabolism
MH  - Mice
MH  - Nerve Tissue Proteins/*metabolism
MH  - Neurons/drug effects/metabolism
MH  - Protein Binding/drug effects
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, trkB/metabolism
MH  - Receptors, AMPA/*metabolism
MH  - Up-Regulation/*drug effects
PMC - PMC3584105
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2013/03/06 06:00
MHDA- 2013/09/04 06:00
PMCR- 2013/02/27
CRDT- 2013/03/06 06:00
PHST- 2012/11/30 00:00 [received]
PHST- 2013/01/17 00:00 [accepted]
PHST- 2013/03/06 06:00 [entrez]
PHST- 2013/03/06 06:00 [pubmed]
PHST- 2013/09/04 06:00 [medline]
PHST- 2013/02/27 00:00 [pmc-release]
AID - PONE-D-12-38051 [pii]
AID - 10.1371/journal.pone.0057124 [doi]
PST - ppublish
SO  - PLoS One. 2013;8(2):e57124. doi: 10.1371/journal.pone.0057124. Epub 2013 Feb 27.