PMID- 24316448
OWN - NLM
STAT- MEDLINE
DCOM- 20140822
LR  - 20201021
IS  - 1873-2747 (Electronic)
IS  - 0361-9230 (Linking)
VI  - 100
DP  - 2014 Jan
TI  - The expression of vesicular glutamate transporter 3 and vesicular monoamine 
      transporter 2 induced by brain-derived neurotrophic factor in dorsal root 
      ganglion neurons in vitro.
PG  - 93-106
LID - S0361-9230(13)00188-3 [pii]
LID - 10.1016/j.brainresbull.2013.11.007 [doi]
AB  - The vesicular glutamate transporter 3 (VGLUT3) and the vesicular monoamine 
      transporter 2 (VMAT2) are expressed in dorsal root ganglion (DRG) neurons and 
      play an important role in packing the neurotransmitter into synaptic vesicles. 
      Brain-derived neurotrophic factor (BDNF) is one of the most profound known 
      regulators of survival in the developing peripheral nervous system (PNS). Whether 
      BDNF regulates the expression of VGLUT3 and VMAT2 in DRG neurons is still 
      unclear. In the present study, primary cultured rat DRG neurons were used to 
      evaluate the effects of BDNF on VGLUT3 and VMAT2 expression. The signaling 
      pathways of the extracellular signal-regulated protein kinase 1/2 (ERK1/2), the 
      phosphatidylinositol 3-kinase (PI3K)/Akt, and the phospholipase C-gamma (PLC-gamma) 
      involved in these effects were also determined. DRG neurons at 48h post-culture 
      were incubated with BDNF and/or ERK1/2 inhibitor PD98059, PI3K inhibitor 
      LY294002, and PLC-gamma inhibitor U73122 for an additional 24h. After that, the 
      neurite growth and growth-associated protein 43 (GAP-43) expressions after 
      different doses of BDNF treatment were determined by immunofluorescent labeling. 
      The expression of mRNA and protein of VGLUT3 and VMAT2 in different experimental 
      conditions was assessed by real-time PCR, immunoblotting, and immunofluorescent 
      labeling, respectively. The results showed that BDNF exposure promoted neurite 
      growth and GAP-43 expression in DRG neurons in a dose-dependent manner. BDNF 
      induced VGLUT3 upregulation through activation of PLC-gamma signaling pathway. 
      Although BDNF administration did not elevate the levels of VMAT2, the block of 
      the PI3K/Akt or PLC-gamma signaling pathways could inhibit VMAT2 expression in DRG 
      neurons in the presence of BDNF. The knockdown of VGLUT3 or VMAT2 gene by siRNA 
      did not affect the BDNF's effects on GAP-43 upregulation and neurite growth. The 
      upregulation of VGLUT3 induced by BDNF might be that BDNF improved neuronal 
      outgrowth status by promoting GAP-43 expression to stimulate neurite elongation. 
      The contribution of distinct VGLUT3 and VMAT2 transporter expression induced by 
      BDNF might be one of the mechanisms that BDNF regulates neuropathic pain. These 
      data imply that BDNF signaling system might be a potential target on modifying 
      distinct transporter-mediated biological effects of primary sensory neurons.
CI  - Copyright (c) 2013 Elsevier Inc. All rights reserved.
FAU - Liu, Dong
AU  - Liu D
AD  - Department of Anatomy, Shandong University School of Medicine, Jinan 250012, 
      China. Electronic address: cyyzld@gmail.com.
FAU - Bi, Yanwen
AU  - Bi Y
AD  - Department of Cardiosurgery, Shandong University Qilu Hospital, Jinan 250012, 
      China. Electronic address: yanwenbi@126.com.
FAU - Liu, Zhen
AU  - Liu Z
AD  - Department of Anatomy, Shandong University School of Medicine, Jinan 250012, 
      China. Electronic address: zhen@sdu.edu.cn.
FAU - Liu, Huaxiang
AU  - Liu H
AD  - Department of Rheumatology, Shandong University Qilu Hospital, Jinan 250012, 
      China. Electronic address: huaxiangliu@hotmail.com.
FAU - Li, Zhenzhong
AU  - Li Z
AD  - Department of Anatomy, Shandong University School of Medicine, Jinan 250012, 
      China. Electronic address: zli@sdu.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131205
PL  - United States
TA  - Brain Res Bull
JT  - Brain research bulletin
JID - 7605818
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Slc17a8 protein, rat)
RN  - 0 (Slc18a2 protein, rat)
RN  - 0 (Vesicular Glutamate Transport Proteins)
RN  - 0 (Vesicular Monoamine Transport Proteins)
SB  - IM
MH  - Animals
MH  - Blotting, Western
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Fluorescent Antibody Technique
MH  - Ganglia, Spinal/metabolism
MH  - Gene Knockdown Techniques
MH  - Neuralgia/metabolism
MH  - Neurons/*metabolism
MH  - RNA, Small Interfering
MH  - Rats
MH  - Rats, Wistar
MH  - Real-Time Polymerase Chain Reaction
MH  - Signal Transduction/*physiology
MH  - Vesicular Glutamate Transport Proteins/*metabolism
MH  - Vesicular Monoamine Transport Proteins/*metabolism
OTO - NOTNLM
OT  - Brain-derived neurotrophic factor
OT  - Dorsal root ganglion
OT  - Neuron
OT  - Vesicular glutamate transporter 3
OT  - Vesicular monoamine transporter 2
EDAT- 2013/12/10 06:00
MHDA- 2014/08/26 06:00
CRDT- 2013/12/10 06:00
PHST- 2013/09/03 00:00 [received]
PHST- 2013/11/11 00:00 [revised]
PHST- 2013/11/27 00:00 [accepted]
PHST- 2013/12/10 06:00 [entrez]
PHST- 2013/12/10 06:00 [pubmed]
PHST- 2014/08/26 06:00 [medline]
AID - S0361-9230(13)00188-3 [pii]
AID - 10.1016/j.brainresbull.2013.11.007 [doi]
PST - ppublish
SO  - Brain Res Bull. 2014 Jan;100:93-106. doi: 10.1016/j.brainresbull.2013.11.007. 
      Epub 2013 Dec 5.