title: Contributions of astrocytes to epileptogenesis following status epilepticus: opportunities for preventive therapy?
abstract: Status epilepticus (SE) is a life threatening condition that often precedes the development of epilepsy. Traditional treatments for epilepsy have been focused on targeting neuronal mechanisms contributing to hyperexcitability, however, approximately 30% of patients with epilepsy do not respond to existing neurocentric pharmacotherapies. A growing body of evidence has demonstrated that profound changes in the morphology and function of astrocytes accompany SE and persist in epilepsy. Astrocytes are increasingly recognized for their diverse roles in modulating neuronal activity, and understanding the changes in astrocytes following SE could provide important clues about the mechanisms underlying seizure generation and termination. By understanding the contributions of astrocytes to the network changes underlying epileptogenesis and the development of epilepsy, we will gain a greater appreciation of the contributions of astrocytes to dynamic circuit changes, which will enable us to develop more successful therapies to prevent and treat epilepsy. This review summarizes changes in astrocytes following SE in animal models and human temporal lobe epilepsy and addresses the functional consequences of those changes that may provide clues to the process of epileptogenesis.
authors.affiliation: Interdepartmental Program in Neuroscience, University of Utah, Salt Lake City, UT, USA.
authors.forename: M B
authors.initials: MB
authors.lastname: Gibbons
authors.forename: R M
authors.initials: RM
authors.lastname: Smeal
authors.forename: D K
authors.initials: DK
authors.lastname: Takahashi
authors.forename: J R
authors.initials: JR
authors.lastname: Vargas
authors.forename: K S
authors.initials: KS
authors.lastname: Wilcox
mesh_terms: D000927:Anticonvulsants / Q000627:therapeutic use; D001253:Astrocytes / Q000378:metabolism / Q000473:pathology*; D001812:Blood-Brain Barrier; D020013:Calcium Signaling; D004827:Epilepsy / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D017470:Receptors, Glutamate / Q000378:metabolism; D013226:Status Epilepticus / Q000150:complications / Q000378:metabolism / Q000473:pathology*
chemical_list: D000927:Anticonvulsants; D017470:Receptors, Glutamate