PMID- 25467984
OWN - NLM
STAT- MEDLINE
DCOM- 20150206
LR  - 20220316
IS  - 1097-4199 (Electronic)
IS  - 0896-6273 (Print)
IS  - 0896-6273 (Linking)
VI  - 84
IP  - 5
DP  - 2014 Dec 3
TI  - Essential role of presynaptic NMDA receptors in activity-dependent BDNF secretion 
      and corticostriatal LTP.
PG  - 1009-22
LID - S0896-6273(14)00965-9 [pii]
LID - 10.1016/j.neuron.2014.10.045 [doi]
AB  - Activation of N-methyl-D-aspartate subtype of glutamate receptors (NMDARs) in 
      postsynaptic dendrites is required for long-term potentiation (LTP) of many 
      excitatory synapses, but the role of presynaptic axonal NMDARs in synaptic 
      plasticity remains to be clarified. Here we report that axonal NMDARs play an 
      essential role in LTP induction at mouse corticostriatal synapses by triggering 
      activity-induced presynaptic secretion of brain-derived neurotrophic factor 
      (BDNF). Genetic depletion of either BDNF or the NMDAR subunit GluN1 specifically 
      in cortical axons abolished corticostriatal LTP in response to theta burst 
      stimulation (TBS). Furthermore, functional axonal NMDARs were required for 
      TBS-triggered prolonged axonal Ca(2+) elevation and BDNF secretion, supporting 
      the notion that activation of axonal NMDARs induces BDNF secretion via enhancing 
      Ca(2+) signals in the presynaptic nerve terminals. These results demonstrate that 
      presynaptic NMDARs are equally important as postsynaptic NMDARs in LTP induction 
      of corticostriatal synapses due to their role in mediating activity-induced 
      presynaptic BDNF secretion.
CI  - Copyright (c) 2014 Elsevier Inc. All rights reserved.
FAU - Park, Hyungju
AU  - Park H
AD  - Division of Neurobiology, Department of Molecular and Cell Biology, Helen Wills 
      Neuroscience Institute, University of California, Berkeley, CA 94720.
FAU - Popescu, Andrei
AU  - Popescu A
AD  - Division of Neurobiology, Department of Molecular and Cell Biology, Helen Wills 
      Neuroscience Institute, University of California, Berkeley, CA 94720.
FAU - Poo, Mu-ming
AU  - Poo MM
AD  - Division of Neurobiology, Department of Molecular and Cell Biology, Helen Wills 
      Neuroscience Institute, University of California, Berkeley, CA 94720; Institute 
      of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of 
      Sciences, Shanghai 200031, China. Electronic address: mpoo@berkeley.edu.
LA  - eng
GR  - R01 NS036999/NS/NINDS NIH HHS/United States
GR  - NS 036999/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20141120
PL  - United States
TA  - Neuron
JT  - Neuron
JID - 8809320
RN  - 0 (Antibodies)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (Luminescent Proteins)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 76326-31-3 (2-amino-5-phosphopentanoic acid)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2)
RN  - HG18B9YRS7 (Valine)
SB  - IM
MH  - Animals
MH  - Antibodies/pharmacology
MH  - Brain-Derived Neurotrophic Factor/genetics/*metabolism
MH  - Calcium-Calmodulin-Dependent Protein Kinase Type 2/genetics
MH  - Cerebral Cortex/*cytology
MH  - Corpus Striatum/*cytology
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - Long-Term Potentiation/drug effects/genetics/*physiology
MH  - Luminescent Proteins/genetics/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - Microscopy, Confocal
MH  - Models, Biological
MH  - Neurons/drug effects/*physiology
MH  - Receptor, trkB/immunology
MH  - Receptors, N-Methyl-D-Aspartate/*metabolism
MH  - Synapses/genetics/*physiology
MH  - Time Factors
MH  - Valine/analogs & derivatives/pharmacology
PMC - PMC4465395
MID - NIHMS639991
EDAT- 2014/12/04 06:00
MHDA- 2015/02/07 06:00
PMCR- 2015/12/03
CRDT- 2014/12/04 06:00
PHST- 2014/10/16 00:00 [accepted]
PHST- 2014/12/04 06:00 [entrez]
PHST- 2014/12/04 06:00 [pubmed]
PHST- 2015/02/07 06:00 [medline]
PHST- 2015/12/03 00:00 [pmc-release]
AID - S0896-6273(14)00965-9 [pii]
AID - 10.1016/j.neuron.2014.10.045 [doi]
PST - ppublish
SO  - Neuron. 2014 Dec 3;84(5):1009-22. doi: 10.1016/j.neuron.2014.10.045. Epub 2014 
      Nov 20.