Effects of MCI-186 on intracellular calcium ion concentration and membrane fluidity of hippocampal neurons in a rat model of Alzheimer's disease  

作　　者：Ming Yu Lei Qin Zhao Wang Xiaohong Lu Ying Zhu Wenhui Leng Xuan Wang 

机构地区：[1]Department of Neurology, Affiliated Hospital of Jiangsu University, Zhenjiang 212001, Jiangsu Province, China [2]Department of Preventive Medicine, Nanjing University of Chinese Medicine, Nanjing 210046, Jiangsu Province, China [3]Department of Biochemistry, Basic Medical College of Jiamusi University, Jiamusi 154007, Heilongjiang Province, China [4]Department of Neurology, Affiliated First Hospital of Jiamusi University, Jiamusi 154002, Heilongjiang Province, China

出　　处：《Neural Regeneration Research》2011年第29期2245-2250,共6页中国神经再生研究（英文版）

基　　金：the Natural Science Foundation of Heilongjiang Province,No.D200807;Projects of Clinical Medicine in Science and Technology Development of Jiangsu University,No.JLY20080013

摘　　要：The present study observed the effects of MCI-186 on the intracellular calcium ion concentration （[Ca2＋]i） and membrane fluidity of hippocampal neurons in Alzheimer＇s disease （AD） model rats to validate the neuroprotective effects of MCI-186. Compared with normal and sham-operated rats, the escape latency was obviously prolonged, spanning platform times were obviously reduced, [Ca2＋]i was increased, and microviscosity η value was increased in AD rats. MCI-186 at 0.5 mg/mL and 0.2 mg/mL obviously shortened escape latency, increased spanning platform times and decreased [Ca2＋]i and microviscosity η values in AD rats at 7 and 17 days after induction of the model. The differences in the above-mentioned indices between normal and MCI-186-treated rats were statistically significant. MCI-186 at 0.2 mg/mL yielded better curative effects than 0.5 mg/mL MCI-186. These findings suggest that MCI-186 improves learning and memory abilities in AD rats by decreasing [Ca2＋]i and increasing membrane fluidity of hippocampal neurons.The present study observed the effects of MCI-186 on the intracellular calcium ion concentration （[Ca2＋]i） and membrane fluidity of hippocampal neurons in Alzheimer＇s disease （AD） model rats to validate the neuroprotective effects of MCI-186. Compared with normal and sham-operated rats, the escape latency was obviously prolonged, spanning platform times were obviously reduced, [Ca2＋]i was increased, and microviscosity η value was increased in AD rats. MCI-186 at 0.5 mg/mL and 0.2 mg/mL obviously shortened escape latency, increased spanning platform times and decreased [Ca2＋]i and microviscosity η values in AD rats at 7 and 17 days after induction of the model. The differences in the above-mentioned indices between normal and MCI-186-treated rats were statistically significant. MCI-186 at 0.2 mg/mL yielded better curative effects than 0.5 mg/mL MCI-186. These findings suggest that MCI-186 improves learning and memory abilities in AD rats by decreasing [Ca2＋]i and increasing membrane fluidity of hippocampal neurons.

关 键 词：MCI-186 Alzheimer＇s disease LEARNING MEMORY calcium ion neurodegenerative diseases neural regeneration 

分 类 号：Q426[生物学—神经生物学] Q26[生物学—生理学]