PMID- 25286195
OWN - NLM
STAT- MEDLINE
DCOM- 20150610
LR  - 20211021
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 9
IP  - 10
DP  - 2014
TI  - Neuronal activity induces synaptic delivery of hnRNP A2/B1 by a BDNF-dependent 
      mechanism in cultured hippocampal neurons.
PG  - e108175
LID - 10.1371/journal.pone.0108175 [doi]
LID - e108175
AB  - Dendritic protein synthesis plays a critical role in several forms of synaptic 
      plasticity, including BDNF (brain-derived neurotrophic factor)-mediated long-term 
      synaptic potentiation (LTP). Dendritic transcripts are typically transported in a 
      repressed state as components of large ribonucleoprotein complexes, and then 
      translated upon stimulation at, or in the vicinity, of activated synapses. 
      Heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNP A2/B1) is a trans-acting 
      factor involved in dendritic mRNA trafficking, but how the distribution of the 
      protein in dendrites is regulated has not been characterized. Here we found that 
      a fraction of hnRNP A2/B1 is present at the synapse under resting conditions in 
      cultured hippocampal neurons. Accordingly, this ribonucleoprotein was detected in 
      free mRNP, monosomal, and polyribosomal fractions obtained from 
      synaptoneurosomes. Neuronal activity and BDNF treatment increased hnRNP A2/B1 
      protein levels in the cell body and dendritic compartments, and induced the 
      delivery of this protein to synaptic sites. The activity-dependent accumulation 
      of hnRNP A2/B1 at the synapse required, at least in part, the activation of TrkB 
      receptors, presumably by BDNF. This neurotrophin also upregulated the hnRNP A2/B1 
      mRNA in the soma but was without effect on the abundance of neuritic hnRNP A2/B1 
      transcripts. These results show that the distribution of hnRNP A2/B1 is regulated 
      by BDNF and by neuronal activity, an effect that may have a role in BDNF-induced 
      synaptic plasticity events.
FAU - Leal, Graciano
AU  - Leal G
AD  - CNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, 
      Portugal; Department of Life Sciences, University of Coimbra, Coimbra, Portugal.
FAU - Afonso, Pedro M
AU  - Afonso PM
AD  - CNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, 
      Portugal; Faculty of Pharmacy, University of Coimbra, Coimbra, Portugal.
FAU - Duarte, Carlos B
AU  - Duarte CB
AD  - CNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, 
      Portugal; Department of Life Sciences, University of Coimbra, Coimbra, Portugal.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20141006
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Disks Large Homolog 4 Protein)
RN  - 0 (Dlg4 protein, rat)
RN  - 0 (Heterogeneous-Nuclear Ribonucleoprotein Group A-B)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (Membrane Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (hnRNP A2)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*metabolism/pharmacology
MH  - Cells, Cultured
MH  - Dendrites/drug effects/metabolism
MH  - Disks Large Homolog 4 Protein
MH  - Heterogeneous-Nuclear Ribonucleoprotein Group A-B/*metabolism
MH  - Hippocampus/*cytology
MH  - Intracellular Signaling Peptides and Proteins/metabolism
MH  - Membrane Proteins/metabolism
MH  - Neurons/drug effects/*metabolism
MH  - Polyribosomes/drug effects/metabolism
MH  - RNA, Messenger/genetics/metabolism
MH  - Rats
MH  - Synapses/*metabolism
MH  - Up-Regulation/drug effects
PMC - PMC4186808
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2014/10/07 06:00
MHDA- 2015/06/11 06:00
PMCR- 2014/10/06
CRDT- 2014/10/07 06:00
PHST- 2014/06/19 00:00 [received]
PHST- 2014/08/26 00:00 [accepted]
PHST- 2014/10/07 06:00 [entrez]
PHST- 2014/10/07 06:00 [pubmed]
PHST- 2015/06/11 06:00 [medline]
PHST- 2014/10/06 00:00 [pmc-release]
AID - PONE-D-14-26982 [pii]
AID - 10.1371/journal.pone.0108175 [doi]
PST - epublish
SO  - PLoS One. 2014 Oct 6;9(10):e108175. doi: 10.1371/journal.pone.0108175. 
      eCollection 2014.