BDNF-TrkB signaling is involved in the histopathological damage, synaptic protein loss and inflammatory response caused by an electromagnetic pulse in rat brain cortex.

Abstract

An electromagnetic pulse (EMP) can cause central nervous system damage, but the underlying mechanisms remain unclear. In this study, we investigated the effects of EMP exposure on the cortex of the rat brain and the involvement of deficiencies in the brain-derived neurotrophic factor (BDNF)-tyrosine receptor kinase B (TrkB) signaling pathway. Rats were exposed to EMPs once a day for 7 consecutive days. Histopathological damage was assessed by hematoxylin and eosin staining. Levels of synaptic marker postsynaptic density protein-95 (PSD95) and synaptophysin (SYN), as well as methyl-CpG-binding protein 2 (Mecp2), were determined by western blots. Levels of the proinflammatory cytokine interleukin-8 and the anti-inflammatory factor interleukin-10 were assessed using enzyme-linked immunosorbent assays. In addition, to examine the BDNF-TrkB signaling pathway, the protein and phosphorylated protein levels of BDNF, pTrkB and TrkB were determined. Our results indicated that EMP exposure led to histopathological damage, the loss of synaptic protein PSD95, Mecp2 overexpression and inflammatory response. Moreover, the BDNF-TrkB pathway was downregulated after EMP exposure. 7,8-Dihydroxyflavone, a TrkB agonist, prevented all of the EMP-induced changes except the Mecp2 overexpression. Taken together, these results suggest that EMP exposure can cause damage to the rat brain cortex and that deficient BDNF-TrkB signaling plays a role in much of the EMP-related damage.