title: Magnetic stimulation modulates structural synaptic plasticity and regulates BDNF-TrkB signal pathway in cultured hippocampal neurons.
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.
authors.affiliation: Deparment of Human Anatomy, Hebei Medical University, Shijiazhuang 050017, Hebei, PR China.
authors.forename: Jun
authors.initials: J
authors.lastname: Ma
authors.forename: Zhanchi
authors.initials: Z
authors.lastname: Zhang
authors.forename: Yuhong
authors.initials: Y
authors.lastname: Su
authors.forename: Lin
authors.initials: L
authors.lastname: Kang
authors.forename: Dandan
authors.initials: D
authors.lastname: Geng
authors.forename: Yanyong
authors.initials: Y
authors.lastname: Wang
authors.forename: Feng
authors.initials: F
authors.lastname: Luan
authors.forename: Mingwei
authors.initials: M
authors.lastname: Wang
authors.forename: Huixian
authors.initials: H
authors.lastname: Cui
mesh_terms: D000199:Actins / Q000096:biosynthesis; D000818:Animals; D017209:Apoptosis / Q000502:physiology; D015153:Blotting, Western; D019208:Brain-Derived Neurotrophic Factor / Q000502:physiology*; D002470:Cell Survival / Q000502:physiology; D002478:Cells, Cultured; D000076122:Disks Large Homolog 4 Protein; D004574:Electromagnetic Fields; D019922:GAP-43 Protein / Q000096:biosynthesis; D051528:Guanylate Kinases / Q000096:biosynthesis; D006624:Hippocampus / Q000502:physiology*; D007150:Immunohistochemistry; D020935:MAP Kinase Signaling System / Q000502:physiology; D008565:Membrane Proteins / Q000096:biosynthesis; D051379:Mice; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000502:physiology*; D019869:Phosphatidylinositol 3-Kinases / Q000502:physiology; D020813:Receptor, trkB / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*; D013569:Synapses / Q000502:physiology; D016708:Synaptophysin / Q000096:biosynthesis / Q000235:genetics; D014158:Transcription, Genetic / Q000502:physiology
chemical_list: D000199:Actins; D019208:Brain-Derived Neurotrophic Factor; D000076122:Disks Large Homolog 4 Protein; C501447:Dlg4 protein, mouse; D019922:GAP-43 Protein; D008565:Membrane Proteins; D016708:Synaptophysin; D019869:Phosphatidylinositol 3-Kinases; D020813:Receptor, trkB; D051528:Guanylate Kinases