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• W2005510359 abstract "Brain-derived neurotrophic factor (BDNF) is known to have important functions in neuronal survival, differentiation, and plasticity. In addition to its role as a survival-promoting factor, BDNF reportedly can enhance neuronal cell death in some cases, for example, the death caused by excitotoxicity or glucose deprivation. The cellular mechanism of the death-enhancing effect of BDNF remains unknown, in contrast to that of its survival-promoting effect. In this work, we found that BDNF markedly accelerated the nitric oxide (NO) donor-induced death of cultured embryonic cortical neurons. BDNF increased the number of cells with nuclear condensation and DNA fragmentation 24 h after treatment with the NO donor, but it did not change the number of those cells 36 h after the treatment. The BDNF-accelerated death of cortical neurons was inhibited by the addition of actinomycin D or cycloheximide. These results suggest that BDNF can accelerate apoptotic cell death elicited by NO donor. TrkB-IgG and K252a blocked the BDNF-induced acceleration of the death, indicating that the death-accelerating effect by BDNF is mediated by TrkB. In addition, the BDNF-accelerated apoptosis was inhibited by the addition of SB202190 and SB203580, specific inhibitors of p38 mitogen-activated protein kinase (MAPK), and U0126, a specific inhibitor of MAPK/ERK kinase 1, indicating that the activation of both p38 MAPK and ERK is involved in the signaling cascade of the BDNF-accelerated, NO donor-induced apoptosis." @default.
• W2005510359 created "2016-06-24" @default.
• W2005510359 creator A5005841735 @default.
• W2005510359 creator A5030034139 @default.
• W2005510359 creator A5060467145 @default.
• W2005510359 date "2002-01-04" @default.
• W2005510359 modified "2023-09-25" @default.
• W2005510359 title "Brain-Derived Neurotrophic Factor Accelerates Nitric Oxide Donor-Induced Apoptosis of Cultured Cortical Neurons" @default.
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• W2005510359 doi "https://doi.org/10.1046/j.1471-4159.2000.0750494.x" @default.
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