CXCR4 antagonist AMD3100 reverses the neurogenesis promoted by enriched environment and suppresses long-term seizure activity in adult rats of temporal lobe epilepsy
CXCR4 antagonist AMD3100 reverses the neurogenesis promoted by enriched environment and suppresses long-term seizure activity in adult rats of temporal lobe epilepsy
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CXCR4拮抗剂AMD3100逆转丰富环境促进的神经发生并抑制成年颞叶癫痫大鼠的长期癫痫发作活动
DOI:
10.1016/j.bbr.2017.01.014
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发表时间:
2017-03
影响因子:
2.7
通讯作者:
Zhao Chuansheng
中科院分区:
文献类型:
--
作者:
Zhou Zhike;Liu Tingting;Sun Xiaoyu;Mu Xiaopeng;Zhu Gang;Xiao Ting;Zhao Mei;Zhao Chuansheng
It has been showed that enriched environment (EE) enhances the hippocampal neurogenesis and improves the cognitive impairments, accompanied by the increased expressions of stromal cell-derived factor-1 (SDF-1) in adult rats of temporal lobe epilepsy (TLE). We examined whether the enhanced neurogenesis and improved cognitive functions induced by EE following seizures were mediated by SDF-1/CXCR4 pathway. Therefore, we investigated the effects of the EE combined with CXCR4 antagonist AMD3100 on neurogenesis, cognitive functions and the long-term seizure activity in the TLE model. Adult rats were randomly assigned as control rats, rats treated with EE, rats subjected to status epilepticus (SE), post-SE rats treated with EE, AMD3100 or EE combined with AMD3100 respectively. We used immunofluorescence staining to analyze the hippocampal neurogenesis and Nissl staining to evaluate hippocampal damage. Electroencephalography was used to measure the frequency and mean duration of spontaneous seizures. Cognitive function was evaluated by Morris water maze test. EE treatment significantly, as well as improved cognitive impairments and decreased long-term seizure activity, and that these effects might be mediated through SDF-1/CXCR4 pathway during the chronic stage of TLE. Although AMD3100 reversed the effect of EE on neurogenesis, it did not abolish the cognitive improvement induced by EE following seizures. More importantly, EE combined with AMD3100 treatment significantly suppressed long-term seizure activity, which provided promising evidences to treat TLE.
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影响因子:
4.7
作者:
通讯作者:
--
影响因子:
8.3
作者:
Niv, Fanny;Keiner, Silke;Redecker, Christoph
通讯作者:
Redecker, Christoph
DOI:
10.1023/b:amai.0000012894.03739.de
发表时间:
2004-12
影响因子:
1.2
作者:
通讯作者:
--
影响因子:
2.5
作者:
R. O’Reilly;Rajan Bhattacharyya;M. Howard;Nicholas A. Ketz
通讯作者:
R. O’Reilly;Rajan Bhattacharyya;M. Howard;Nicholas A. Ketz
影响因子:
3.1
作者:
Chen CC;Hsu YH;Jayaseema DM;Chen JY;Hueng DY;Chang C
通讯作者:
Chang C