PMID- 24934279
OWN - NLM
STAT- MEDLINE
DCOM- 20150721
LR  - 20141113
IS  - 1743-1328 (Electronic)
IS  - 0161-6412 (Linking)
VI  - 37
IP  - 1
DP  - 2015 Jan
TI  - TrkB is involved in the mechanism by which BDNF accelerates the glutamate-induced 
      death of rat neuroblastoma B35 cells.
PG  - 30-4
LID - 10.1179/1743132814Y.0000000403 [doi]
AB  - OBJECTIVE: Brain-derived neurotrophic factor (BDNF) binds to its high-affinity 
      binding receptor, tropomyosin-related kinase (Trk) B, and can induce neuronal 
      differentiation and survival. BDNF also accelerates neuronal cell death in a 
      glutamate-induced model; however, it has been unknown whether the mechanism 
      involves TrkB. In the current study, to determine the role of TrkB in neuronal 
      cell death, we investigated TrkB involvement in BDNF acceleration of 
      glutamate-induced neuronal death. METHODS: A TrkB-stable transformant of rat 
      neuroblastoma B35 (B35(TrkB)) cells was utilized to investigate whether TrkB is 
      involved in BDNF acceleration of neuronal death. The cell viability of the 
      B35(TrkB) cells was compared to that of mock vector-transgened B35 (B35(mock)) 
      cells after treatment with/without BDNF and glutamate. RESULTS: In both B35(TrkB) 
      and B35(mock) cells, glutamate treatment decreased the cell viability. BDNF 
      treatment further accelerated the decrease in the viability of B35(TrkB) cells, 
      but not that in the viability of B35(mock) cells. At glutamate concentrations 
      that did not significantly decrease cell viability, BDNF increased the cell 
      viability of B35(TrkB), but not that of B35(mock). A mitogen-activated protein 
      kinase (MAPK) inhibitor, U0126, suppressed BDNF's accelerating effect on cell 
      death. Although B35 parental cells endogenously express other neurotrophin 
      receptors such as TrkA, nerve growth factor beta (a ligand of TrkA and p75(NTR)) 
      could not influence the viability of B35(TrkB) or B35(mock) cells. CONCLUSION: 
      These results indicate that TrkB is an intermediator for the trophic and 
      toxicity-exacerbating effects of BDNF against cell viabilities at non-cytotoxic 
      and cytotoxic glutamate concentrations, respectively.
FAU - Maki, Takehiro
AU  - Maki T
FAU - Arishima, Kazuyoshi
AU  - Arishima K
FAU - Yamamoto, Masako
AU  - Yamamoto M
FAU - Sakaue, Motoharu
AU  - Sakaue M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140616
PL  - England
TA  - Neurol Res
JT  - Neurological research
JID - 7905298
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Butadienes)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Nitriles)
RN  - 0 (U 0126)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - 9061-61-4 (Nerve Growth Factor)
RN  - EC 2.7.10.1 (Receptor, trkA)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Butadienes/pharmacology
MH  - Cell Death/drug effects/*physiology
MH  - Cell Line, Tumor
MH  - Cell Survival/drug effects/physiology
MH  - Enzyme Inhibitors/pharmacology
MH  - Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors/metabolism
MH  - Glutamic Acid/*metabolism
MH  - Nerve Growth Factor/metabolism
MH  - Neuroblastoma/physiopathology
MH  - Neurons/drug effects/*physiology
MH  - Nitriles/pharmacology
MH  - Rats
MH  - Receptor, trkA/metabolism
MH  - Receptor, trkB/genetics/*metabolism
OTO - NOTNLM
OT  - BDNF,
OT  - Glutamate,
OT  - NGFbeta,
OT  - Neuronal cell death,
OT  - TrkB,
OT  - p75NTR
EDAT- 2014/06/18 06:00
MHDA- 2015/07/22 06:00
CRDT- 2014/06/18 06:00
PHST- 2014/06/18 06:00 [entrez]
PHST- 2014/06/18 06:00 [pubmed]
PHST- 2015/07/22 06:00 [medline]
AID - 10.1179/1743132814Y.0000000403 [doi]
PST - ppublish
SO  - Neurol Res. 2015 Jan;37(1):30-4. doi: 10.1179/1743132814Y.0000000403. Epub 2014 
      Jun 16.