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Introduction

  • Denson G. Fujikawa
Chapter

Abstract

In the early 1980s it was recognized that excessive Ca2+ influx, presumably through voltage-gated Ca2+ channels, with a resultant increase in intracellular Ca2+, was associated with neuronal death from cerebral ischemia, hypoglycemia, and status epilepticus (Siejö 1981). Calcium activation of phospholipases, with arachidonic acid accumulation and its oxidation, generating free radicals, was thought to be a potential mechanism by which neuronal damage occurs. In cerebral ischemia and hypoglycemia, energy failure was thought to be the reason for excessive Ca2+ influx, whereas in status epilepticus it was thought that repetitive depolarizations were responsible (Siejö 1981).

Keywords

Cerebral Ischemia Status Epilepticus Neuronal Death Kainic Acid Monosodium Glutamate 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media, LLC 2010

Authors and Affiliations

  1. 1.Neurology DepartmentVA Greater Los Angeles Healthcare SystemNorth HillsUSA
  2. 2.Department of Neurology and Brain Research InstituteDavid Geffen School of Medicine, University of CaliforniaLos AngelesUSA

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