Open AccessEnriched Environment Altered Aberrant Hippocampal Neurogenesis and Improved Long-Term Consequences After Temporal Lobe Epilepsy in Adult Rats
Author(s) -
Xiaoqian Zhang,
Tingting Liu,
Zhike Zhou,
Xiaopeng Mu,
Chengguang Song,
Ting Xiao,
Mei Zhao,
Chuansheng Zhao
Publication year - 2015
Publication title -
journal of molecular neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.936
H-Index - 86
eISSN - 1559-1166
pISSN - 0895-8696
DOI - 10.1007/s12031-015-0571-0
Subject(s) - neurogenesis , hippocampal formation , hippocampus , status epilepticus , neuroscience , epilepsy , psychology , temporal lobe , morris water navigation task , environmental enrichment , epileptogenesis , dentate gyrus , nissl body , endocrinology , medicine , biology , pathology , staining
Abnormal hippocampal neurogenesis is thought to contribute to cognitive impairments in chronic temporal lobe epilepsy (TLE). Stromal cell-derived factor-1 (SDF-1) and its specific receptor CXCR4 play important roles in neurogenesis. We investigated whether enriched environment (EE) might be beneficial for TLE. Adult rats were randomly assigned as control rats, rats subjected to status epilepticus (SE), or post-SE rats treated with EE for 30 days. We used immunofluorescence staining to analyze the hippocampal neurogenesis and Nissl staining to evaluate hippocampal damage. Electroencephalography was used to measure the duration of spontaneous seizures. Cognitive function was evaluated by Morris water maze. Western blot was used to measure the expression of SDF-1 and CXCR4 in the hippocampus. In the present study, we found the TLE model resulted in aberrant neurogenesis such as reduced proliferation, intensified dendritic development of newborn neurons, as well as spontaneous seizures and cognitive impairments. More importantly, EE treatment significantly increased the cell proliferation and survival, extended the apical dendrites, and delayed the attenuation of the expression of SDF-1 and CXCR4, accompanied by decreased long-term seizure activity and improved cognitive impairments in adult rats after TLE. These results provided morphological evidence that EE might be beneficial for treating TLE.