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磁刺激调节培养海马神经元的结构型突触可塑性,并调节 BDNF-TrkB 信号通路。

Magnetic stimulation modulates structural synaptic plasticity and regulates BDNF-TrkB signal pathway in cultured hippocampal neurons.

机构信息

Deparment of Human Anatomy, Hebei Medical University, Shijiazhuang 050017, Hebei, PR China.

出版信息

Neurochem Int. 2013 Jan;62(1):84-91. doi: 10.1016/j.neuint.2012.11.010. Epub 2012 Nov 28.

DOI:10.1016/j.neuint.2012.11.010
PMID:23201339
Abstract

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.

摘要

重复经颅磁刺激(rTMS)是一种神经精神工具,可用于研究学习和认知功能的神经生物学。很少有研究检查低频(⩽1Hz)磁刺激(MS)对体外神经元结构突触可塑性的影响,因此,本研究检查了其对海马神经元和突触形态以及突触蛋白标志物和信号通路的影响。同样,低频磁场刺激(1Hz)的两种强度都激活了脑源性神经营养因子(BDNF)和原肌球蛋白相关激酶 B(TrkB)途径,包括丝裂原活化蛋白激酶(MAPK)/细胞外信号调节激酶(ERK)途径和磷酸肌醇 3-激酶(PI3K)/蛋白激酶 B(Akt)途径。具体而言,低强度磁场刺激(LIMS,1.14Tesla,1Hz)促进了更广泛的树突和轴突分支,以及增加了突触密度、增厚 PSD(突触后密度)和上调突触小体蛋白(SYN)、生长相关蛋白 43(GAP43)和突触后密度 95(PSD95)。相反,高强度磁场刺激(HIMS,1.55Tesla,1Hz)似乎有害,减少了树突和轴突分支,并导致明显的结构损伤,包括 PSD 变薄、突触减少和突触结构紊乱,以及 GAP43 和 PSD95 的上调,可能是因为它们有能力减轻功能障碍。总之,我们推断低频磁场刺激通过激活 BDNF-TrkB 信号通路参与调节海马神经元的结构突触可塑性。

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