• Sun Seek Min, Jihua An, Ji-Hye Lee, Geun Hee Seol, Jae Hyeung Im, Hye-Sun Kim, Tai-Kyoung Baik, and Ran-Sook Woo.
• Department of Physiology and Biophysics, College of Medicine, Eulji University, Daejeon, Republic of Korea.
• Neurosci. Lett. 2011 Nov 7;505(1):6-9.

AbstractNeuregulin-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 β (Aβ) peptide is generally believed to play a critical role in the pathogenesis of AD. The present study examined the effect of synthetic Aβ₁₋₄₂ 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 Aβ₁₋₄₂ (200 nM) significantly inhibited the development of LTP without affecting basal synaptic transmission. Pretreatment with NRG1 effectively prevented Aβ₁₋₄₂-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 Aβ-induced hippocampal LTP impairment, suggesting that NRG1 may be a promising candidate for the treatment of early-stage AD.Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.

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