Protein kinase C mediates the amyloid β-protein fragment 31-35-Induced suppression of hippocampal la

• 作 者: Jun-FangZHANG;Jin-ShunQI;Jian-TianQIAO;
• 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年期

　　Alzheimers disease (AD) is the most common cause of dementia in the elderly,characterized mostly by cognitive deficits and progressive loss of memory.Amyloid β (Aβ) protein is widely thought to play a critical role in pathogenesis of AD.Long-term potentiation (LTP) is a persistent enhancement of excitatory synaptic transmission induced by some kinds of preceding operations of high-frequency stimulation (HFS) and hippocampal LTP is usually used as an electrophysiological model of memory.Our previous experiments indicated that both Aβ25-35 and A1331-35 could strongly impair hippocampal synaptic plasticity in vivo by suppressing the maintenance of late phase of LTP (L-LTP).To further investigate whether the suppression of L-LTP by Aβ 31-35 is involved in the alteration of intracellular protein kinase C (PKC) level,the effects of PMA (phorbol 12-myristate 13-acetate),a PKC agonist,and chelerythrine chloride,a PKC antagonist,on the multiple group of high frequency stimulation (HFS) induced L-LTP were observed in the present study.