Study on the induction of in vivo hippocampal long-term depression and its modulation by amyloid β-p

• 作 者: Li CHENG Jin-Shun QI
• 机 构: Department of Physiology, Shanxi Medical University, Taiyuan 030001, China
• 出 处: 中国神经科学学会第四次会员代表大会暨第七届全国学术会议(The 7th Biennial Meeting and the
• 发表日期: 2007年12期
• 关键词: Alzheimer's disease (AD) amyloid-β peptide (AβP) AβP31-35 Aβ25-35 long-term

　　Accumulation and deposition of amyloid-β peptide (Aβ P) in brain areas have been widely believed to play a critical role in the pathogenesis of Alzheimer s disease (AD).AβP may be responsible for much of the learning and memory deficit seen early in the disease by interfering with synaptic plasticity in the brain.It is reported that application of relatively low concentrations of Aβ P or some of its fragments,such as AβP25-35,can block the high-frequency stimulation (HFS)-induced long-term potentiation (LTP) of synaptic transmission in hippocampus.Our previous study indicates that AβP31-35,a shorter fragment of AβP,could also suppress the LTP in hippocampal CA1 area.Long-term depression (LTD) induced by low-frequency stimulation (LFS) is another type of cellular model for studying learning and memory,but whether it is affected by AβP in AD is still an open question now.