Protective effect of nicotine on the cultured rat basal forebrain neurons damaged by β-Amyloid (Aβ)25-35 protein cytotoxicity

OBJECTIVE: We sought to investigate the intervention effect of nicotine on beta-amyloid (A beta)25-35 protein cytotoxicity in the rat basal forebrain neurons primary cultures. MATERIALS AND METHODS: For this purpose, freshly isolated rat basal forebrain neurons were cultured for 7 days and then exposed to either A beta(25-35) or the combination of A beta(25-35) and nicotine for 48 hours. The effects of A beta(25-35) and nicotine on neurons morphology, growth status and TrkA expression were evaluated through microscopy, MTT assay, RTPCR and immunocytochemistry. RESULTS: We found that the exposure of cultured neurons to A beta(25-35) resulted in remarkable morphological changes. The average process number and length as well as the maximum process length of neurons were significantly decreased as compared with those of control. MTT assay showed that A beta(25-35) impaired the growth of neurons. A beta(25-35) also inhibited the expression of TrkA at both mRNA and protein levels. However, the addition of nicotine significantly attenuated these changes, indicating that nicotine could protect the neurons from the cytotoxicity of A beta(25-35). CONCLUSIONS: Nicotine could be useful for the treatment of Alzheimer's disease through its ability to rescue the neurons from A beta(25-35) cytotoxicity and the protective effect involved upregulated expression of TrkA receptors.