Chapter

Programmed Necrosis after Status Epilepticus

Jerome Niquet, Maria-Leonor Lopez-Meraz and Claude G. Wasterlain

in Jasper's Basic Mechanisms of the Epilepsies

Fourth edition

Published on behalf of ©Jeffrey L. Noebels, Massimo Avoli, Michael A. Rogawski, Richard W. Olsen, and Antonio V. Delgado-Escueta

Published in print July 2012 | ISBN: 9780199746545
Published online April 2013 | e-ISBN: 9780199322817 | DOI: http://dx.doi.org/10.1093/med/9780199746545.003.0029

Series: Contemporary Neurology Series

Programmed Necrosis after Status Epilepticus

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In this review, we will discuss the most recent advances in the field of neuronal injury following epileptic seizures, with an emphasis on the mechanism of neuronal necrosis. The ultrastructure of cell death and the ubiquity of endogenous cell death programs were first described in the 1970s, and the two main categories of cell death, apoptosis and necrosis, were originally defined according to morphological criteria.1 The role of glutamate and its analogues in excitotoxic cell death, and the concept of excitotoxicity—including its role in seizures—derived from the pioneering studies of John Olney and his disciples.2–5 Multiple cell death factors and cell death programs have been identified in developmental and disease-induced neuronal apoptosis,6–8 and there is mounting clinical and experimental evidence of their contribution to seizure-induced neuronal injury.9–16 Because these death factors were originally identified in classic apoptosis, any form of cell death in which they are expressed is often called apoptotic, even if its morphology suggests necrosis. This has caused considerable confusion in the literature and should be discouraged.17–20 In this chapter, we will discuss the involvement of cell death factors in morphologically defined necrosis, the main mode of status epilepticus (SE)-induced cell death in the adult and even in the developing brain. We find that necrosis is frequently an active form of neuronal death, requiring the expression or activation of some of the same cell death factors usually identified with apoptosis. While this finding raises the hope that targeting common cell death pathways might have therapeutic benefits for both necrosis and apoptosis, the multiplicity and redundancy of cell death pathways for both modes of neuronal death also raise formidable problems when we consider the potential therapeutic applications of these mechanisms.

Chapter.  5663 words.  Illustrated.

Subjects: Neurology

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