Altered expression of c-Abl in patients with epilepsy and in a rat model
Article first published online: 2 APR 2014
Copyright © 2014 Wiley Periodicals, Inc.
Volume 68, Issue 7, pages 306–316, July 2014
How to Cite
Chen, L., Wang, Z., Tang, B., Fang, M., Li, J., Chen, G. and Wang, X. (2014), Altered expression of c-Abl in patients with epilepsy and in a rat model. Synapse, 68: 306–316. doi: 10.1002/syn.21741
- Issue published online: 12 MAY 2014
- Article first published online: 2 APR 2014
- Accepted manuscript online: 13 MAR 2014 12:22AM EST
- Manuscript Accepted: 8 MAR 2014
- Manuscript Revised: 18 FEB 2014
- Manuscript Received: 12 NOV 2013
- temporal lobe epilepsy;
c-Abl is an ubiquitous nonreceptor tyrosine kinase involved in signal transduction pathways that promote cytoskeleton remodeling and apoptosis. In brain, c-Abl plays important roles in neuronal development, neurogenesis, neuronal migration, neurite outgrowth, and synaptic plasticity. Neuronal death, gliosis and synaptic remodeling are thought to be involved in the development of epilepsy. Here we investigated the expression pattern and distribution of total and phosphorylated c-Abl in patients with temporal lobe epilepsy (TLE) and a rat model of epilepsy to explore the probable relationship between c-Abl expression and TLE. Double immunolabeling, Immunohistochemistry, and immunoblotting results showed that both total and phosphorylated c-Abl were upregulated in the temporal neocortex of 26 patients with TLE compared to nonepileptic controls. In the temporal neocortex of pilocarpine-treated rats, upregulation of total and phosphorylated c-Abl began 6 hours after seizures, with relatively high expression for 60 days. In the hippocampus of experimental rats, total unphosphorylated c-Abl elevated from 6 hours to 30 days after seizures, the expression then returned to normal levels at 60 days, while phosphorylated c-Abl increased along with the time and maintained at significant high levels for up to 60 days. These results indicate that c-Abl may play an important role in the development of TLE. Synapse 68:306–316, 2014. © 2014 Wiley Periodicals, Inc.