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Previous Article | Next Article
The Journal of Neuroscience, October 15, 1998, 18(20):8382-8393
Patterns of Status Epilepticus-Induced Neuronal Injury during Development and Long-Term Consequences
Raman Sankar1, 2, 3, Don H. Shin1, 2, 3, Hantao Liu1, 3, Andrey Mazarati1, 3, Anne Pereira de Vasconcelos4, and Claude G. Wasterlain1, 3 Departments of 1 Neurology and 2 Pediatrics, University of California Los Angeles School of Medicine, Los Angeles, California 90095-1752, 3 Epilepsy Research Laboratories, Veterans Affairs Medical Center, Sepulveda, California 91343, and 4 Institut National de la Santé et de la Recherche Médicale U 398, 67085 Strasbourg, France
The lithium-pilocarpine model of status epilepticus (SE) was used to study the type and distribution of seizure-induced neuronal injury in the rat and its consequences during development. Cell death was evaluated in hematoxylin- and eosin-stained sections and by electron microscopy. Damage to the CA1 neurons was maximal in the 2- and 3-week-old pups and decreased as a function of age. On the other hand, damage to the hilar and CA3 neurons was minimal in the 2-week-old rat pups but reached an adult-like pattern in the 3-week-old animals, and damage to amygdalar neurons increased progressively with age. The 3-week-old animals also demonstrated vulnerability of the dentate granule cells. To evaluate neuronal apoptosis, we used terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling (TUNEL) stain, confocal fluorescence microscopy of ethidium bromide-stained sections, electron microscopy, and DNA electrophoresis. Neurons displaying all of those features of apoptotic death in response to SE were seen in the CA1 region of the 2-week-old pups and in the hilar border of the dentate granule cells of the 3-week-old animals. Some (3/11) of the animals that underwent SE at 2 weeks of age and most of the animals that underwent SE at 3 or 4 weeks of age (8/11 and 6/8, respectively) developed spontaneous seizures later in life; the latter showed SE-induced synaptic reorganization as demonstrated by Timm methodology. These results provide strong evidence for the vulnerability of the immature brain to seizure-induced damage, which bears features of both necrotic and apoptotic death and contributes to synaptic reorganization and the development of chronic epilepsy.
Key words: status epilepticus; seizures; lithium; pilocarpine; hippocampus; apoptosis; necrosis; mossy fiber sprouting; epileptogenesis; rats; development
Copyright © 1998 Society for Neuroscience 0270-6474/98/18208382-12$05.00/0
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