[Frontiers in Bioscience S3, 565-593, January 1, 2011]

Epileptiform activity in the limbic system

Mauro S. Oliveira1, Luis F. Pacheco2, Carlos F. Mello3, Esper A. Cavalheiro4, Emilio R. Garrido-Sanabriasup>2

1Federal University of Pampa at Itaqui, Itaqui 97650-000, RS, Brazil, 2Department of Biological Sciences at the University of Texas at Brownsville and Center for Biomedical Studies, 80 Fort Brown, Brownsville, Texas 78520, USA, 3Department of Physiology and Pharmacology, Center of Health Sciences, Federal University of Santa Maria, Santa Maria 97105-900, RS, Brazil, 4Laboratory of Experimental Neurology, Department of Neurology and Neurosurgery, Federal University of Sao Paulo, São Paulo 04023-900, SP, Brazil


1. Abstract
2. Introduction
3. Models of convulsions versus models exhibiting recurrent spontaneous seizures
3.1. Chronic epilepsy models with limbic epileptogenesis
3.2. Electrically-induced animal models to investigate MTLE
3.3. Self-sustained limbic status epilepticus models
3.3.1. In vivo epileptiform activity in hippocampus during pilocarpine-induced status epilepticus
3.3.2. In vivo epileptiform activity during pilocarpine-induced spontaneous recurrent seizures
3.3.3. In vitro epileptiform activity in slices obtained from pilocarpine-treated epileptic animals
3.3.4. In vitro models of acute epileptiform activy in limbic structures from normal animals
4. Genetic versus acquired channelopathies
5. MTLE as an acquired channelopathy
5.1. Potassium channels
5.2. Voltage-gated sodium channels
5.3. Voltage-gated calcium channels
5.4. Cyclic nucleotide-regulated channels
6. Summary and perspectives
7. Acknowledgments
8. References


Mesial temporal lobe epilepsy (MTLE) is a common neurological disorder characterized by hyperexcitability of limbic structures. Studies in epileptic patients and animal models of MTLE indicate that epileptiform activity arise primarily from limbic areas (e.g. hippocampus) with secondary propagation to cortical areas. A wealth of evidence indicates that epileptiform activity is associated with complex patterns in the expression and function of ion channels, receptors and transporters. Accordingly, several studies portrait MTLE as a post-transcriptional acquired channelopathy. The present review describes the most common features of epileptiform activity emerging from animal models of limbic epileptogenesis and critically discusses the supporting evidence that MTLE is a complex acquired channelopathy.