Epileptogenic roles of astroglial death and regeneration in the dentate gyrus of experimental temporal lobe epilepsy
Article first published online: 14 JUL 2006
Copyright © 2006 Wiley-Liss, Inc.
Volume 54, Issue 4, pages 258–271, September 2006
How to Cite
Kang, T.-C., Kim, D.-S., Kwak, S.-E., Kim, J.-E., Won, M. H., Kim, D.-W., Choi, S.-Y. and Kwon, O.-S. (2006), Epileptogenic roles of astroglial death and regeneration in the dentate gyrus of experimental temporal lobe epilepsy. Glia, 54: 258–271. doi: 10.1002/glia.20380
- Issue published online: 24 JUL 2006
- Article first published online: 14 JUL 2006
- Manuscript Accepted: 2 JUN 2006
- Manuscript Revised: 23 MAY 2006
- Manuscript Received: 20 MAR 2006
- Korea Science and Engineering Foundation, Korea Research Foundation. Grant Numbers: R01-2005-000-10004-0, M103KV010020-06K2201-02010, KRF-2005-015-E00003
- P2X7 receptor
Recent studies have demonstrated that blockade of neuronal death in the hippocampus cannot prevent epileptogenesis in various epileptic models. These reports indicate that neurodegeneration alone is insufficient to cause epilepsy, and that the role of astrocytes in epileptogenesis should be reconsidered. Therefore, the present study was designed to elucidate whether altered morphological organization or the functionalities of astrocytes induced by status epilepticus (SE) is responsible for epileptogenesis. Glial responses (reactive microgliosis followed by astroglial death) in the dentate gyrus induced by pilocarpine-induced SE were found to precede neuronal damage and these alterations were closely related to abnormal neurotransmission related to altered vesicular glutamate and GABA transporter expressions, and mossy fiber sprouting in the dentate gyrus. In addition, newly generated astrocytes showed down-regulated expressions of glutamine synthase, glutamate dehydrogenase, and glial GABA transporter. Taken together, our findings suggest that glial responses after SE may contribute to epileptogenesis and the acquisition of the properties of the epileptic hippocampus. Thus, we believe that it is worth considering new therapeutic approaches to epileptogenesis involving targeting the inactivation of microglia and protecting against astroglial loss. © 2006 Wiley-Liss, Inc.