期刊
EPILEPSY & BEHAVIOR
卷 7, 期 2, 页码 190-203出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.yebeh.2005.06.003
关键词
astrocytes; gene expression; hippocampal sclerosis; interleukin-1 beta; molecular biology of epilepsy; seizures
资金
- NINDS NIH HHS [NS 048434] Funding Source: Medline
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R21NS048434] Funding Source: NIH RePORTER
This review summarizes the salient features of the anatomical and molecular neuropathology of the hippocampus from patients with intractable temporal lobe epilepsy (TLE). It argues that sclerotic hippocampus is essential for seizure expression and that sclerosis is not a consequence of seizures, but is related to the epileptogenicity of the seizure focus. While neurons in sclerotic hippocampus may contribute to hippocampal hyperexcitability, this role is perhaps less important than that of the astrocytes. The astrocytes in sclerotic hippocampus may directly influence excitability through altered water homeostasis and K+ buffering by redistribution of AQP4 transporters on their plasma membrane. It is proposed that they contribute to a high extracellular glutamate level through reduced glutamine synthetase, and activation through pro-inflammatory factors that release chemokines and cytokines, which enhance calcium-dependent glutamate release. Such a focal pool of glutamate may diffuse to surrounding neuron-rich areas to generate seizure activity in TLE. (c) 2005 Elsevier Inc. All rights reserved.
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