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. 2018 Feb 13;9:50. doi: 10.3389/fneur.2018.00050

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Copyright © 2018 Baek, Kim, Pyo, Jung, Park, Kim and Cho.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic diagram of the therapeutic mechanisms of repetitive magnetic stimulation (rMS) following ischemia/reperfusion (I/R) injury. High-frequency rMS increases cell proliferation and mediates the protective effects against apoptosis induced by I/R injury. In addition to enhancing the Ca²⁺–calmodulin-dependent protein kinase II (CaMKII)–cAMP-response element binding protein (CREB) signaling pathway by high-frequency rMS, it also results in activation of brain-derived neurotrophic factor (BDNF) expression and synaptic plasticity in I/R injury.