PMID- 23201339
OWN - NLM
STAT- MEDLINE
DCOM- 20130604
LR  - 20220310
IS  - 1872-9754 (Electronic)
IS  - 0197-0186 (Linking)
VI  - 62
IP  - 1
DP  - 2013 Jan
TI  - Magnetic stimulation modulates structural synaptic plasticity and regulates 
      BDNF-TrkB signal pathway in cultured hippocampal neurons.
PG  - 84-91
LID - S0197-0186(12)00371-3 [pii]
LID - 10.1016/j.neuint.2012.11.010 [doi]
AB  - Repetitive transcranial magnetic stimulation (rTMS) is a neuropsychiatric tool 
      that can be used to investigate the neurobiology of learning and cognitive 
      function. Few studies have examined the effects of low frequency (⩽1Hz) magnetic 
      stimulation (MS) on structural synaptic plasticity of neurons in vitro, thus, the 
      current study examined its effects on hippocampal neuron and synapse morphology, 
      as well as synaptic protein markers and signaling pathways. Similarly, both 
      intensities of low frequency magnetic stimulation (1Hz) activated brain-derived 
      neurotrophic factor (BDNF) and tropomyosin-related kinase B (TrkB) pathways, 
      including the pathways for mitogen-activated protein kinase (MAPK)/extracellular 
      signal-regulated kinase (ERK) and for phosphoinositide 3-kinase (PI3K)/protein 
      kinase B (Akt). Specifically, low intensity magnetic stimulation (LIMS, 
      1.14Tesla, 1Hz) promoted more extensive dendritic and axonal arborization, as 
      well as increasing synapses density, thickening PSD (post synaptic density) and 
      upregulation of synaptophysin (SYN), growth associated protein 43 (GAP43) and 
      post synaptic density 95 (PSD95). Conversely, high intensity magnetic stimulation 
      (HIMS, 1.55Tesla, 1Hz) appeared to be detrimental, reducing dendritic and axonal 
      arborization and causing apparent structural damage, including thinning of PSD, 
      less synapses and disordered synaptic structure, as well as upregulation of GAP43 
      and PSD95, possibly for their ability to mitigate dysfunction. In conclusion, we 
      infers that low frequency magnetic stimulation participates in regulating 
      structural synaptic plasticity of hippocampal neurons via the activation of 
      BDNF-TrkB signaling pathways.
CI  - Copyright (c) 2012 Elsevier Ltd. All rights reserved.
FAU - Ma, Jun
AU  - Ma J
AD  - Deparment of Human Anatomy, Hebei Medical University, Shijiazhuang 050017, Hebei, 
      PR China.
FAU - Zhang, Zhanchi
AU  - Zhang Z
FAU - Su, Yuhong
AU  - Su Y
FAU - Kang, Lin
AU  - Kang L
FAU - Geng, Dandan
AU  - Geng D
FAU - Wang, Yanyong
AU  - Wang Y
FAU - Luan, Feng
AU  - Luan F
FAU - Wang, Mingwei
AU  - Wang M
FAU - Cui, Huixian
AU  - Cui H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20121128
PL  - England
TA  - Neurochem Int
JT  - Neurochemistry international
JID - 8006959
RN  - 0 (Actins)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Disks Large Homolog 4 Protein)
RN  - 0 (Dlg4 protein, mouse)
RN  - 0 (GAP-43 Protein)
RN  - 0 (Membrane Proteins)
RN  - 0 (Synaptophysin)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - EC 2.7.4.8 (Guanylate Kinases)
SB  - IM
MH  - Actins/biosynthesis
MH  - Animals
MH  - Apoptosis/physiology
MH  - Blotting, Western
MH  - Brain-Derived Neurotrophic Factor/*physiology
MH  - Cell Survival/physiology
MH  - Cells, Cultured
MH  - Disks Large Homolog 4 Protein
MH  - *Electromagnetic Fields
MH  - GAP-43 Protein/biosynthesis
MH  - Guanylate Kinases/biosynthesis
MH  - Hippocampus/*physiology
MH  - Immunohistochemistry
MH  - MAP Kinase Signaling System/physiology
MH  - Membrane Proteins/biosynthesis
MH  - Mice
MH  - Neuronal Plasticity/*physiology
MH  - Neurons/*physiology
MH  - Phosphatidylinositol 3-Kinases/physiology
MH  - Receptor, trkB/*physiology
MH  - Signal Transduction/*physiology
MH  - Synapses/physiology
MH  - Synaptophysin/biosynthesis/genetics
MH  - Transcription, Genetic/physiology
EDAT- 2012/12/04 06:00
MHDA- 2013/06/05 06:00
CRDT- 2012/12/04 06:00
PHST- 2012/08/01 00:00 [received]
PHST- 2012/11/07 00:00 [revised]
PHST- 2012/11/16 00:00 [accepted]
PHST- 2012/12/04 06:00 [entrez]
PHST- 2012/12/04 06:00 [pubmed]
PHST- 2013/06/05 06:00 [medline]
AID - S0197-0186(12)00371-3 [pii]
AID - 10.1016/j.neuint.2012.11.010 [doi]
PST - ppublish
SO  - Neurochem Int. 2013 Jan;62(1):84-91. doi: 10.1016/j.neuint.2012.11.010. Epub 2012 
      Nov 28.