Fenghua Zhao and Yida Hu contributed equally to this work.
Abnormal expression of stathmin 1 in brain tissue of patients with intractable temporal lobe epilepsy and a rat model
Article first published online: 23 MAY 2012
Copyright © 2012 Wiley Periodicals, Inc.
Volume 66, Issue 9, pages 781–791, September 2012
How to Cite
Zhao, F., Hu, Y., Zhang, Y., Zhu, Q., Zhang, X., Luo, J., Xu, Y. and Wang, X. (2012), Abnormal expression of stathmin 1 in brain tissue of patients with intractable temporal lobe epilepsy and a rat model. Synapse, 66: 781–791. doi: 10.1002/syn.21567
- Issue published online: 3 JUL 2012
- Article first published online: 23 MAY 2012
- Accepted manuscript online: 25 APR 2012 11:08PM EST
- Manuscript Accepted: 17 APR 2012
- Manuscript Received: 23 FEB 2012
- National Natural Science Foundation of China. Grant Number: 81071039
- Chongqing Municipal Health Bureau (Key Projects)
- Chongqing Municipal Health Bureau (Two-rivers scholar training funds)
- temporal lobe epilepsy;
- stathmin 1;
- microtubule dynamics;
- neurite elongation
Microtubule dynamics have been shown to contribute to neurite outgrowth, branching, and guidance. Stathmin 1 is a potent microtubule-destabilizing factor that is involved in the regulation of microtubule dynamics and plays an essential role in neurite elongation and synaptic plasticity. Here, we investigate the expression of stathmin 1 in the brain tissues of patients with intractable temporal lobe epilepsy (TLE) and experimental animals using immunohistochemistry, immunofluorescence and western blotting. We obtained 32 temporal neocortex tissue samples from patients with intractable TLE and 12 histologically normal temporal lobe tissues as controls. In addition, 48 Sprague Dawley rats were randomly divided into six groups, including one control group and five groups with epilepsy induced by lithium chloride-pilocarpine. Hippocampal and temporal lobe tissues were obtained from control and epileptic rats on Days 1, 7, 14, 30, and 60 after kindling. Stathmin 1 was mainly expressed in the neuronal membrane and cytoplasm in the human controls, and its expression levels were significantly higher in patients with intractable TLE. Moreover, stathmin 1 was also expressed in the neurons of both the control and the experimental rats. Stathmin 1 expression was decreased in the experimental animals from 1 to 14 days postseizure and then significantly increased at Days 30 and 60 compared with the control group. Many protruding neuronal processes were observed in the TLE patients and in the chronic stage epileptic rats. These data suggest that stathmin 1 may participate in the abnormal network reorganization of synapses and contribute to the pathogenesis of TLE. Synapse 66:781–791, 2012. © 2012 Wiley Periodicals, Inc.