PMID- 19794395
OWN - NLM
STAT- MEDLINE
DCOM- 20100302
LR  - 20211020
IS  - 1559-7016 (Electronic)
IS  - 0271-678X (Print)
IS  - 0271-678X (Linking)
VI  - 30
IP  - 2
DP  - 2010 Feb
TI  - Brain-derived neurotrophic factor enhances the expression of the monocarboxylate 
      transporter 2 through translational activation in mouse cultured cortical 
      neurons.
PG  - 286-98
LID - 10.1038/jcbfm.2009.208 [doi]
AB  - MCT2 is the predominant neuronal monocarboxylate transporter allowing lactate use 
      as an alternative energy substrate. It is suggested that MCT2 is upregulated to 
      meet enhanced energy demands after modifications in synaptic transmission. 
      Brain-derived neurotrophic factor (BDNF), a promoter of synaptic plasticity, 
      significantly increased MCT2 protein expression in cultured cortical neurons (as 
      shown by immunocytochemistry and western blot) through a translational regulation 
      at the synaptic level. Brain-derived neurotrophic factor can cause translational 
      activation through different signaling pathways. Western blot analyses showed 
      that p44/p42 mitogen-activated protein kinase (MAPK), Akt, and S6 were strongly 
      phosphorylated on BDNF treatment. To determine by which signal transduction 
      pathway(s) BDNF mediates its upregulation of MCT2 protein expression, the effect 
      of specific inhibitors for p38 MAPK, phosphoinositide 3-kinase (PI3K), mammalian 
      target of rapamycin (mTOR), mitogen-activated protein kinase (MAPK)/extracellular 
      signal-regulated kinase (ERK) kinase (MEK), p44/p42 MAPK (ERK), and Janus kinase 
      2 (JAK2) was evaluated. It could be observed that the BDNF-induced increase in 
      MCT2 protein expression was almost completely blocked by all inhibitors, except 
      for JAK2. These data indicate that BDNF induces an increase in neuronal MCT2 
      protein expression by a mechanism involving a concomitant stimulation of 
      PI3K/Akt/mTOR/S6, p38 MAPK, and p44/p42 MAPK. Moreover, our observations suggest 
      that changes in MCT2 expression could participate in the process of synaptic 
      plasticity induced by BDNF.
FAU - Robinet, Camille
AU  - Robinet C
AD  - Department of Physiology, University of Lausanne, Lausanne, Switzerland.
FAU - Pellerin, Luc
AU  - Pellerin L
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090930
PL  - United States
TA  - J Cereb Blood Flow Metab
JT  - Journal of cerebral blood flow and metabolism : official journal of the 
      International Society of Cerebral Blood Flow and Metabolism
JID - 8112566
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Monocarboxylic Acid Transporters)
RN  - 0 (Slc16a7 protein, mouse)
SB  - IM
MH  - Animals
MH  - Blotting, Western
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Cells, Cultured
MH  - Cerebral Cortex/drug effects/metabolism
MH  - Enzyme Inhibitors/pharmacology
MH  - Gene Expression
MH  - *Gene Expression Regulation
MH  - Immunohistochemistry
MH  - Mice
MH  - Monocarboxylic Acid Transporters/*biosynthesis/genetics
MH  - Neuronal Plasticity/drug effects/physiology
MH  - Neurons/drug effects/*metabolism
MH  - *Protein Biosynthesis/drug effects
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Signal Transduction/drug effects/*physiology
PMC - PMC2949129
EDAT- 2009/10/02 06:00
MHDA- 2010/03/03 06:00
PMCR- 2011/02/01
CRDT- 2009/10/02 06:00
PHST- 2009/10/02 06:00 [entrez]
PHST- 2009/10/02 06:00 [pubmed]
PHST- 2010/03/03 06:00 [medline]
PHST- 2011/02/01 00:00 [pmc-release]
AID - jcbfm2009208 [pii]
AID - 10.1038/jcbfm.2009.208 [doi]
PST - ppublish
SO  - J Cereb Blood Flow Metab. 2010 Feb;30(2):286-98. doi: 10.1038/jcbfm.2009.208. 
      Epub 2009 Sep 30.