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• W1136692988 abstract "Chemicals that induce limbic hyperactivity which generalizes into a status epilepticus cause severe neurodegeneration in limbic-related structures (piriform cortex, amygdala, and CA1 and CA3 regions of the hippocampus) [1–5]. Two examples are soman (O-1,2,2-trimethylpropyl methylphosphono-fluoridate), an irreversible acetylcholinesterase inhibitor, and kainic acid (KA), a glutamate analog. KA-induced seizures occur first in the ventral hippocampus and lateral septum; the areas where increases in local cerebral glucose use (LCGU) occur first after injection of KA. They are also the only areas where increases in LCGU occur when the spread of electrical activity from the initiation sites is prevented by diazepam pretreatment [6]. In contrast, when the spread of electrical activity in soman exposed rats is prevented by diazepam pretreatment, increases in LCGU, occur in the globus pallidus, ventral pallidum and substantia nigra [7]. Although the seizure-initiation sites for these two agents are different, eventually the spread of seizure activity via enhanced glutamate release within limbic-related structures leads to hyperactivity which generalizes throughout the brain causing a full-blown status epilepticus. Furthermore, the neuropathology associated with both chemical agents are similar [1–5]. LCGU dramatically increases in many brain regions, including limbic-related areas during the seizure phase induced by either soman or KA [1–5]. The increased neuronal activity causes a calcium stress leading to production of reactive oxygen species which contributes to the neuropathology [8]." @default.
• W1136692988 created "2016-06-24" @default.
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• W1136692988 date "1999-01-01" @default.
• W1136692988 modified "2023-09-25" @default.
• W1136692988 title "Metallothionein-1,2 and heme oxygenase-1 are expressed in damaged brain regions following chemically-induced seizures" @default.
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• W1136692988 doi "https://doi.org/10.1007/978-3-0348-8847-9_50" @default.
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