TY - JOUR ID - 8837 TI - Allicin attenuates tunicamycin-induced cognitive deficits in rats via its synaptic plasticity regulatory activity JO - Iranian Journal of Basic Medical Sciences JA - IJBMS LA - en SN - 2008-3866 AU - Xiang, Qiong AU - Li, Xian-hui AU - Yang, Bo AU - Fang, Xin-xing AU - Jia, Jing AU - Ren, Jie AU - Dong, Yu-chun AU - Ou-Yang, Cheng AU - Wang, Guang-cheng AD - Institute of Medicine, Medical Research Center, Jishou University, Hunan, China AD - Jishou University First Affiliated Hospital, Jishou University, Hunan, China AD - College of Chemistry and Chemical Engineering, Jishou University, Hunan, China Y1 - 2017 PY - 2017 VL - 20 IS - 6 SP - 676 EP - 682 KW - Allicin KW - Dendritic spine density KW - fEPSP KW - Hippocampus KW - Synaptic plasticity DO - 10.22038/ijbms.2017.8837 N2 - 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: 200–250 g male SD rats were divided into three groups at random: control group (n=12), TM group (5 μl, 50 μM, i.c.v, n=12), and allicin treatment group (180 mg/kg/d with chow diet, n=12). After 16 weeks of allicin treatment, the learning ability and memory were tested using novel object recognition (NOR) testing on rats with 72 hr TM treatment (5 μl, 50 μM, i.c.v); meanwhile, the variation of field excitatory postsynaptic potential (fEPSP) in the Schaffer Collateral (SC)-CA1 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-1(GluR1) 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. UR - https://ijbms.mums.ac.ir/article_8837.html L1 - https://ijbms.mums.ac.ir/article_8837_0c2a8003af09d62c03b6c54501b936cf.pdf ER -