PMID- 24302729
OWN - NLM
STAT- MEDLINE
DCOM- 20140317
LR  - 20211021
IS  - 1083-351X (Electronic)
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 289
IP  - 3
DP  - 2014 Jan 17
TI  - Brain-derived neurotrophic factor (BDNF)-induced mitochondrial motility arrest 
      and presynaptic docking contribute to BDNF-enhanced synaptic transmission.
PG  - 1213-26
LID - 10.1074/jbc.M113.526129 [doi]
AB  - Appropriate mitochondrial transport and distribution are essential for neurons 
      because of the high energy and Ca(2+) buffering requirements at synapses. 
      Brain-derived neurotrophic factor (BDNF) plays an essential role in regulating 
      synaptic transmission and plasticity. However, whether and how BDNF can regulate 
      mitochondrial transport and distribution are still unclear. Here, we find that in 
      cultured hippocampal neurons, application of BDNF for 15 min decreased the 
      percentage of moving mitochondria in axons, a process dependent on the activation 
      of the TrkB receptor and its downstream PI3K and phospholipase-Cgamma signaling 
      pathways. Moreover, the BDNF-induced mitochondrial stopping requires the 
      activation of transient receptor potential canonical 3 and 6 (TRPC3 and TRPC6) 
      channels and elevated intracellular Ca(2+) levels. The Ca(2+) sensor Miro1 plays 
      an important role in this process. Finally, the BDNF-induced mitochondrial 
      stopping leads to the accumulation of more mitochondria at presynaptic sites. 
      Mutant Miro1 lacking the ability to bind Ca(2+) prevents BDNF-induced 
      mitochondrial presynaptic accumulation and synaptic transmission, suggesting that 
      Miro1-mediated mitochondrial motility is involved in BDNF-induced mitochondrial 
      presynaptic docking and neurotransmission. Together, these data suggest that 
      mitochondrial transport and distribution play essential roles in BDNF-mediated 
      synaptic transmission.
FAU - Su, Bo
AU  - Su B
AD  - From the Department of Neurobiology, Shandong Provincial Key Laboratory of Mental 
      Disorders, School of Medicine, Shandong University, Jinan, Shandong 250012, 
      China.
FAU - Ji, Yun-Song
AU  - Ji YS
FAU - Sun, Xu-lu
AU  - Sun XL
FAU - Liu, Xiang-Hua
AU  - Liu XH
FAU - Chen, Zhe-Yu
AU  - Chen ZY
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131203
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Mitochondrial Proteins)
RN  - 0 (TRPC Cation Channels)
RN  - 0 (TRPC3 cation channel)
RN  - 0 (Trpc6 protein, rat)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - EC 3.6.5.2 (Rhot1 protein, rat)
RN  - EC 3.6.5.2 (rho GTP-Binding Proteins)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Axons/*metabolism
MH  - Biological Transport, Active/physiology
MH  - Brain-Derived Neurotrophic Factor/genetics/*metabolism
MH  - Calcium/metabolism
MH  - Cells, Cultured
MH  - Enzyme Activation/physiology
MH  - Hippocampus/cytology/*metabolism
MH  - Mitochondria/genetics/*metabolism
MH  - Mitochondrial Proteins/genetics/metabolism
MH  - Mutation
MH  - Phosphatidylinositol 3-Kinases/genetics/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, trkB/genetics/metabolism
MH  - Synaptic Transmission/*physiology
MH  - TRPC Cation Channels/genetics/metabolism
MH  - rho GTP-Binding Proteins/genetics/metabolism
PMC - PMC3894308
OTO - NOTNLM
OT  - Brain-derived Neurotrophic Factor (BDNF)
OT  - Mitochondrial Transport
OT  - Signal Transduction
OT  - Synaptic Plasticity
OT  - TRP Channels
EDAT- 2013/12/05 06:00
MHDA- 2014/03/19 06:00
PMCR- 2015/01/17
CRDT- 2013/12/05 06:00
PHST- 2013/12/05 06:00 [entrez]
PHST- 2013/12/05 06:00 [pubmed]
PHST- 2014/03/19 06:00 [medline]
PHST- 2015/01/17 00:00 [pmc-release]
AID - S0021-9258(20)33604-8 [pii]
AID - M113.526129 [pii]
AID - 10.1074/jbc.M113.526129 [doi]
PST - ppublish
SO  - J Biol Chem. 2014 Jan 17;289(3):1213-26. doi: 10.1074/jbc.M113.526129. Epub 2013 
      Dec 3.