Pulsed electromagnetic field enhances brain-derived neurotrophic factor expression through L-type voltage-gated calcium channel- and erk-dependent signaling pathways in neonatal rat dorsal root ganglion neurons.
Author: Li Y1, Yan X2, Liu J3, Li L4, Hu X5, Sun H6, Tian J7.
Affiliation:
1Second Clinical Medical College, Southern Medical University, Guangzhou 510280, P. R. China. 2Department of Orthopaedics, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, P. R. China. 3Department of Clinical Aerospace Medicine, Fourth Military Medical University, Xi'an 710032, P. R. China. 4Department of Geriatrics,ShaanxiProvincialTCMHospital,Xi'an 710032, P. R. China. 5Department of Endocrinology,ShaanxiProvincialTCMHospital,Xi'an 710032, P. R. China. 6Department of Orthopaedics, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, P. R. China. Electronic address: sunhhi@163.com. 7Second Clinical Medical College, Southern Medical University, Guangzhou 510280, P. R. China. Electronic address: tian_jing6723@aliyun.com.
Conference/Journal: Neurochem Int.
Date published: 2014 Jun 14
Other:
Pages: S0197-0186(14)00143-0 , Special Notes: doi: 10.1016/j.neuint.2014.06.004 , Word Count: 188
Although pulsed electromagnetic field (PEMF) exposure has been reported to promote neuronal differentiation, the mechanism is still unclear. Here, we aimed to examine the effects of PEMF exposure on brain-derived neurotrophic factor (Bdnf) mRNA expression and the correlation between the intracellular free calcium concentration ([Ca2+]i) and Bdnf mRNA expression in cultured dorsal root ganglion neurons (DRGNs). Exposure to 50 Hz and 1 mT PEMF for 2 h increased the level of [Ca2+]i and Bdnf mRNA expression, which was found to be mediated by increased [Ca2+]i from Ca2+ influx through L-type voltage-gated calcium channels (VGCCs). However, calcium mobilization was not involved in the increased [Ca2+]i and BDNF expression, indicating that calcium influx was one of the key factors responding to PEMF exposure. Moreover, PD098059, an extracellular signal-regulated kinase (Erk) inhibitor, strongly inhibited PEMF-dependant Erk1/2 activation and BDNF expression, indicating that Erk activation is required for PEMF-induced upregulation of BDNF expression. These findings indicated that PEMF exposure increased BDNF expression in DRGNs by activating Ca2+- and Erk-dependent signaling pathways.
Copyright © 2014. Published by Elsevier Ltd.
KEYWORDS:
Brain-derived neurotrophic factor; Calcium; Dorsal root ganglion neurons; Electromagnetic field; Erk inhibitor
PMID: 24937769
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