Altered structure and function of astrocytes following status epilepticus

Epilepsy Behav. 2015 Aug:49:17-9. doi: 10.1016/j.yebeh.2015.05.002. Epub 2015 Jul 26.

Abstract

Temporal lobe epilepsy (TLE) is a devastating seizure disorder that is often caused by status epilepticus (SE). Temporal lobe epilepsy can be very difficult to control with currently available antiseizure drugs, and there are currently no disease-modifying therapies that can prevent the development of TLE in those patients who are at risk. While the functional changes that occur in neurons following SE and leading to TLE have been well studied, only recently has research attention turned to the role in epileptogenesis of astrocytes, the other major cell type of the brain. Given that epilepsy is a neural circuit disorder, innovative ways to evaluate the contributions that both neurons and astrocytes make to aberrant circuit activity will be critical for the understanding of the emergent network properties that result in seizures. Recently described approaches using genetically encoded calcium-indicating proteins can be used to image dynamic calcium transients, a marker of activity in both neurons and glial cells. It is anticipated that this work will lead to novel insights into the process of epileptogenesis at the network level and may identify disease-modifying therapeutic targets that have been missed because of a largely neurocentric view of seizure generation following SE. This article is part of a Special Issue entitled "Status Epilepticus".

Keywords: Astrocytes; GCaMP; Status epilepticus; Temporal lobe epilepsy.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Astrocytes / pathology*
  • Brain / pathology*
  • Brain / physiopathology
  • Cell Shape / physiology
  • Disease Models, Animal
  • Epilepsy, Temporal Lobe / pathology*
  • Epilepsy, Temporal Lobe / physiopathology
  • Humans
  • Neurons / pathology*
  • Status Epilepticus / pathology*
  • Status Epilepticus / physiopathology