期刊
NEUROSCIENCE LETTERS
卷 505, 期 1, 页码 6-9出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2011.05.246
关键词
Alzheimer's disease; Amyloid beta peptide; Hippocampus; Long-term potentiation; Neuregulin; ErbB4
资金
- National Research Foundation of Korea [NRF-2009-0074146]
- Korean Government [KRF-2008-331-E00292]
- NRF
- MEST [2009-0085840]
- National Research Foundation of Korea [2009-0085840] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Neuregulin-1 (NRG1) participates in numerous neurodevelopmental processes and plasticity of the brain. Despite this, little is known about its role in Alzheimer's disease (AD). Amyloid eta (A beta) peptide is generally believed to play a critical role in the pathogenesis of AD. The present study examined the effect of synthetic A beta(1-42) peptides on long-term potentiation (LTP) in the CA1 region of mice hippocampal slices, a cellular model of learning and memory. We found that application of a test dose of A beta(1-42) (200 nM) significantly inhibited the development of LIP without affecting basal synaptic transmission. Pretreatment with NRG1 effectively prevented A beta(1-42)-induced impairment of LTP, an effect that was dose-dependent. This LTP-restoring action of NRG1 was almost completely abolished by blocking ErbB4, a key NRG1 receptor, suggesting that NRG1 acts through ErbB4 to exert its protective action on LTP. The present study thus provides the first demonstration that NRG1/ErbB4 protects against A beta-induced hippocampal LTP impairment, suggesting that NRG1 may be a promising candidate for the treatment of early-stage AD. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
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