PMID- 11701755
OWN - NLM
STAT- MEDLINE
DCOM- 20011207
LR  - 20190630
IS  - 0022-3042 (Print)
IS  - 0022-3042 (Linking)
VI  - 79
IP  - 3
DP  - 2001 Nov
TI  - Brain-derived neurotrophic factor enhances depolarization-evoked glutamate 
      release in cultured cortical neurons.
PG  - 522-30
AB  - Brain-derived neurotrophic factor (BDNF) has been reported to play an important 
      role in neuronal plasticity. In this study, we examined the effect of BDNF on an 
      activity-dependent synaptic function in an acute phase. First, we found that 
      short-term treatment (10 min) with BDNF enhanced depolarization-evoked glutamate 
      release in cultured cortical neurons. The enhancement diminished gradually 
      according to the length of BDNF treatment. The BDNF-enhanced release did not 
      require the synthesis of protein and mRNA. Both tetanus toxin and bafilomycin 
      abolished the depolarization-evoked glutamate release with or without BDNF, 
      indicating that BDNF acted via an exocytotic pathway. Next, we investigated the 
      effect of BDNF on intracellular Ca(2+). BDNF potentiated the increase in 
      intracellular Ca(2+) induced by depolarization. The Ca(2+) was derived from 
      intracellular stores, because thapsigargin completely inhibited the potentiation. 
      Furthermore, both thapsigargin and xestospongin C inhibited the effect of BDNF. 
      These results suggested that the release of Ca(2+) from intracellular stores 
      mediated by the IP(3) receptor was involved in the BDNF-enhanced glutamate 
      release. Last, it was revealed that the enhancement of glutamate release by BDNF 
      was dependent on the TrkB-PLC-gamma pathway. These results clearly demonstrate 
      that short-term treatment with BDNF enhances an exocytotic pathway by 
      potentiating the accumulation of intracellular Ca(2+) through intracellular 
      stores.
FAU - Matsumoto, T
AU  - Matsumoto T
AD  - Division of Protein Biosynthesis, Institute for Protein Research, Osaka 
      University, Suita, Osaka, Japan.
FAU - Numakawa, T
AU  - Numakawa T
FAU - Adachi, N
AU  - Adachi N
FAU - Yokomaku, D
AU  - Yokomaku D
FAU - Yamagishi, S
AU  - Yamagishi S
FAU - Takei, N
AU  - Takei N
FAU - Hatanaka, H
AU  - Hatanaka H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Isoenzymes)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - EC 3.1.4.- (Type C Phospholipases)
RN  - EC 3.1.4.3 (Phospholipase C gamma)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*pharmacology
MH  - Calcium/metabolism
MH  - Cells, Cultured
MH  - Cerebral Cortex/cytology
MH  - Evoked Potentials/drug effects
MH  - Exocytosis/drug effects
MH  - Glutamic Acid/*metabolism
MH  - Isoenzymes/metabolism
MH  - Neuronal Plasticity/drug effects
MH  - Neurons/drug effects/*physiology
MH  - Phospholipase C gamma
MH  - Rats
MH  - Receptor, trkB/metabolism
MH  - Type C Phospholipases/metabolism
EDAT- 2001/11/10 10:00
MHDA- 2002/01/05 10:01
CRDT- 2001/11/10 10:00
PHST- 2001/11/10 10:00 [pubmed]
PHST- 2002/01/05 10:01 [medline]
PHST- 2001/11/10 10:00 [entrez]
AID - 10.1046/j.1471-4159.2001.00591.x [doi]
PST - ppublish
SO  - J Neurochem. 2001 Nov;79(3):522-30. doi: 10.1046/j.1471-4159.2001.00591.x.