Modulation of dendritic spines in epilepsy: Cellular mechanisms and functional implications

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Abstract

Epilepsy patients often suffer from significant neurological deficits, including memory impairment, behavioral problems, and psychiatric disorders. While the causes of neuropsychological dysfunction in epilepsy are multifactorial, accumulating evidence indicates that seizures themselves may directly cause brain injury. Although seizures sometimes result in neuronal death, they may also cause more subtle pathological changes in neuronal structure and function, including abnormalities in synaptic transmission. Dendritic spines receive a majority of the excitatory synaptic inputs to cortical neurons and are critically involved in synaptic plasticity and learning. Studies of human epilepsy and experimental animal models demonstrate that seizures may directly affect the morphological and functional properties of dendritic spines, suggesting that seizure-related changes in spines may represent a mechanistic basis for cognitive deficits in epilepsy. Novel therapeutic strategies directed at modulation of spine motility may prevent the detrimental effects of seizures on cognitive function in epilepsy.

Original languageEnglish
Pages (from-to)569-577
Number of pages9
JournalEpilepsy and Behavior
Volume7
Issue number4
DOIs
StatePublished - Dec 2005

Keywords

  • Actin
  • Dendritic spine
  • Epilepsy
  • Learning disability
  • Long-term potentiation
  • Mental retardation
  • Seizure
  • Synaptic transmission

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