Qiong Xiang - Institute of Medicine, Medical Research Center, Jishou University, Hunan, China
Xian-hui Li - Institute of Medicine, Medical Research Center, Jishou University, Hunan, China
Bo Yang - Jishou University First Affiliated Hospital, Jishou University, Hunan, China
Xin-xing Fang - Institute of Medicine, Medical Research Center, Jishou University, Hunan, China
Jing Jia - Institute of Medicine, Medical Research Center, Jishou University, Hunan, China
Jie Ren - Institute of Medicine, Medical Research Center, Jishou University, Hunan, China
Yu-chun Dong - Institute of Medicine, Medical Research Center, Jishou University, Hunan, China
Cheng Ou-Yang - Institute of Medicine, Medical Research Center, Jishou University, Hunan, China
Guang-cheng Wang - College of Chemistry and Chemical Engineering, Jishou University, Hunan, China

Objective(s): To illuminate the functional effects of allicin on rats with cognitive deficits induced by tunicamycin (TM) and the molecular mechanism of this process. Materials and Methods: ۲۰۰–۲۵۰ g male SD rats were divided into three groups at random: control group (n=۱۲), TM group (۵ μl, ۵۰ μM, i.c.v, n=۱۲), and allicin treatment group (۱۸۰ mg/kg/d with chow diet, n=۱۲). After ۱۶ weeks of allicin treatment, the learning ability and memory were tested using novel object recognition (NOR) testing on rats with ۷۲ hr TM treatment (۵ μl, ۵۰ μM, i.c.v); meanwhile, the variation of field excitatory postsynaptic potential (fEPSP) in the Schaffer Collateral (SC)-CA۱ synapse was detected by extracellular electrophysiological recordings and the morphology of dendritic spine was observed by Golgi staining as well as detecting several synaptic plasticity-related proteins by Western blot. Results: The density of dendritic spine was increased significantly in allicin-treated groups and the correspondence slope of fEPSP in TM-induced cognitive deficits group was enhanced and expression of synaptophysin and glutamate receptor-۱(GluR۱) in hippocampal neurons was up-regulated. Conclusion: The results indicate that allicin plays an important role in synaptic plasticity regulation. These finding showed that allicin could be used as a pharmacologic treatment in TM-induced cognitive deficits.

Allicin, Dendritic spine density, fEPSP, Hippocampus, Synaptic plasticity