Lithium chloride administration prevents spatial learning and memory impairment in repeated cerebral ischemia-reperfusion mice by depressing apoptosis and increasing BDNF expression in hippocampus
| Autor: | Xin Jiang, Yanqiu Jia, Jing Xu, Yining Xiao, Mingyue Fan, Wei Jin, Nan Meng, Yu Yin, Haifeng Zhao, Peiyuan Lv |
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| Rok vydání: | 2015 |
| Předmět: |
Carotid Artery Diseases
Male medicine.medical_specialty Cell Survival Ischemia Morris water navigation task Apoptosis CREB Hippocampus Neuroprotection Brain Ischemia Random Allocation Behavioral Neuroscience chemistry.chemical_compound Internal medicine medicine Animals Memory impairment Cyclic AMP Response Element-Binding Protein Maze Learning Nootropic Agents Spatial Memory bcl-2-Associated X Protein Neurons Memory Disorders biology Learning Disabilities business.industry Brain-Derived Neurotrophic Factor medicine.disease Mice Inbred C57BL Disease Models Animal medicine.anatomical_structure Endocrinology Proto-Oncogene Proteins c-bcl-2 chemistry Reperfusion Injury biology.protein Lithium chloride Neuron Lithium Chloride business Neuroscience |
| Zdroj: | Behavioural Brain Research. 291:399-406 |
| ISSN: | 0166-4328 |
| Popis: | Lithium has been reported to have neuroprotective effects, but the preventive and treated role on cognition impairment and the underlying mechanisms have not been determined. In the present study, C57Bl/6 mice were subjected to repeated bilateral common carotid artery occlusion to induce the learning and memory deficits. 2 mmol/kg or 5 mmol/kg of lithium chloride (LiCl) was injected intraperitoneally per day before (for 7 days) or post (for 28 days) the operation. This repeated cerebral ischemia-reperfusion (IR) induced dynamic overexpression of ratio of Bcl-2/Bax and BDNF in hippocampus of mice. LiCl pretreatment and treatment significantly decreased the escape latency and increased the percentage of time that the mice spent in the target quadrant in Morris water maze. 2 mmol/kg LiCl evidently reversed the morphologic changes, up-regulated the survival neuron count and increased the BDNF gene and protein expression. 5 mmol/kg pre-LiCl significantly increased IR-stimulated reduce of Bcl-2/Bax and p-CREB/CREB. These results described suggest that pre-Li and Li treatment may induce a pronounced prevention on cognitive impairment. These effects may relay on the inhibition of apoptosis and increasing BDNF and p-CREB expression. |
| Databáze: | OpenAIRE |
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