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Programmed Neuronal Necrosis and Status Epilepticus
Author(s) -
Niquet Jerome,
Liu Hantao,
Wasterlain Claude G.
Publication year - 2005
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1167.2005.01025.x
Subject(s) - status epilepticus , necrosis , dentate gyrus , apoptosis , cytochrome c , programmed cell death , mitochondrion , biology , pathology , microbiology and biotechnology , neuroscience , chemistry , hippocampus , biochemistry , medicine , epilepsy , genetics
Summary: We examined the mechanism of neuronal necrosis induced by hypoxia in dentate gyrus cultures or by status epilepticus (SE) in adult mice. Our observations showed that hypoxic necrosis can be an active process starting with early mitochondrial swelling and loss of the mitochondrial membrane potential, followed by cytochrome c release and caspase‐9–dependent activation of caspase‐3. This sequence of events (or program) was independent of protein synthesis and may be induced by energy failure and/or calcium overloading of mitochondria. We called this form of necrosis “programmed necrosis.” After SE in adult mice, CA1 and CA3 pyramidal neurons displayed a necrotic morphology, associated with caspase‐3 immunoreactivity and with double‐stranded DNA breaks, suggesting that “programmed necrosis” may be involved in SE‐induced neuronal loss.