Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3052717 | Epilepsy Research | 2010 | 9 Pages |
Abstract
While different hypotheses have been proposed to explain the mechanism of onset of temporal lobe epilepsy (TLE), most of them are based on structural, electrophysiological, cellular or molecular changes in one particular area. Extensive neuronal loss, axon reorganization, dendrite and dendritic spine growth make it impossible to apply one hypothesis to explain epileptogenesis for patients or animal models with different pathophysiological changes in the brain. It is therefore hypothesized that cyto-, axo- and dendro-architectonic changes at multiple brain regions may be involved in epileptogenesis in TLE. In the review, structural changes of the limbic system, in particular, hippocampus, entorhinal cortex, subiculum and amygdale, in the mouse pilocarpine model of TLE will be summarized. Their functional significance will be discussed. The final conclusion and future research directions will then be made.
Keywords
HBDsIMLPSA-NCAMTLEIPISRSMTSMTLENPYPHA-LMFSGluR1LSDPhaseolus vulgaris leucoagglutininInitial precipitating injuryBLAPRHCTBbasolateral amygdalaBDNFmesial temporal sclerosishippocampal sclerosiskainic acidGamma aminobutyric acidElectroencephalographyepileptogenesisstatus epilepticusSPECTfunctional magnetic resonance imagingfMRIStructural changessingle photon emission computed tomographyPositron emission tomographymossy fiber sproutinglateral septumtemporal lobe epilepsyBrain-derived neurotrophic factorlentEntorhinal cortexlateral entorhinal cortexperirhinal cortexinner molecular layerVentral subiculumdorsal subiculumpolysialylated neural cell adhesion moleculeEEGParvalbuminPETChATCalretinincalbindincholera toxin B subunitcholine acetyltransferaseGABAglutamate receptor 1Neuropeptide Y
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Authors
Feng Ru Tang, Weng Keong Loke,