Kainic acid induced seizures: Neurochemical and histopathological changes

Sperk, Günther; Lassmann, Hans; Baran, Halina; Kish, Stephen J.; Seitelberger, F; Hornykiewicz, Oleh

doi:10.1016/0306-4522(83)90113-6

Cited by 514 publications

(315 citation statements)

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“…Regardless of age, all FVB mice observed to be in status epilepticus, exhibited the well-documented acute neuropathologic response to convulsant doses of KA (Nadler et al, 1980a,b;Schwob et al, 1980;Nadler, 1981;Coyle, 1983;Sperk et al, 1983;Ben-Ari, 1985;Jarrard and Meldrum, 1993;Olney, 1994), while no obvious damage was observed in C57BL/6 mice. While the mechanisms whereby neuronal cells die following an excitotoxic insult are not fully understood, it has been hypothesized that a variety of cascades involving biochemical and electrophysiological events combine to produce neuronal damage (Choi, 1992;Whetsell, 1996;Michaelis, 1998;Nicholls and Budd, 1998;Sattler and Tymianski, 2000).…”

Section: Discussionmentioning

confidence: 99%

Effect of age on kainate-induced seizure severity and cell death

et al. 2008

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While the onset and extent of epilepsy increases in the aged population, the reasons for this increased incidence remain unexplored. The present study used two inbred strains of mice (C57BL/6J and FVB/NJ) to address the genetic control of age-dependent neurodegeneration by building upon previous experiments that have identified phenotypic differences in susceptibility to hippocampal seizure-induced cell death. We determined if seizure induction and seizure-induced cell death are affected differentially in young adult, mature, and aged male C57BL/6J and FVB/NJ mice administered the excitotoxin, kainic acid. Dose response testing was performed in three-four groups of male mice from each strain. Following kainate injections, mice were scored for seizure activity and brains from mice in each age group were processed for light microscopic histopathologic evaluation seven days following kainate administration to evaluate the severity of seizure-induced brain damage. Irrespective of the dose of kainate administered or the age group examined, resistant strains of mice (C57BL/6J) continued to be resistant to seizure-induced cell death. In contrast, aged animals of the FVB/NJ strain were more vulnerable to the induction of behavioral seizures and associated neuropathology after systemic injection of kainic acid than young or middle-aged mice.Results from these studies suggest that the age-related increased susceptibility to the neurotoxic effects of seizure induction and seizure-induced injury is regulated in a strain-dependent manner, similar to previous observations in young adult mice. Keywords mouse strain; excitotoxicity; kainic acid; epilepsy; cell death; aging Knowledge about the influence of aging on the susceptibility of the brain to seizure disorders is of critical importance in geriatric medicine and public health. Epilepsy is the most common neurological disorder after stroke, affecting more than 50 million persons worldwide and with a 2-3% life time risk of being given a diagnosis of epilepsy (Browne and Holmes, 2001). Currently it is well known that there is a significant incidence of epilepsy in children. However, less clearly recognized but of increasing importance is the significant incidence of epilepsy in Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript the elderly population. Recent studies in the United States and Europe indicate that the agespecific incidence of epilepsy is higher in those over the age of 65 years than in those in the first decade of life (Talli...

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Section: Discussionmentioning

confidence: 99%

Effect of age on kainate-induced seizure severity and cell death

et al. 2008

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“…5-AV did not attenuate KA-induced c-Fos and c-Jun IR in the hippocampus. The increases of c-Fos and c-Jun induced by KA might be a marker in seizure activity, excitotoxicity or the activation of target genes (Sperk et al, 1983;Kitayama et al, 1999;Won et al, 2000). Zhang et al suggest that c-Fos is a genetic regulator for cellular mechanisms controlling neuronal excitability and survival (Zhang et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

“…Administration of KA at a convulsant dose induces c-Fos, Fra and Jun in rat hippocampus and entorhinal cortex (Le Gal La Salle, 1988;Popovici et al, 1990;Pennypacker et al, 1993). The increases of c-Fos and c-Jun induced by KA might be a marker in seizure activity, excitotoxicity or the activation of target genes (Sperk et al, 1983;Kitayama et al, 1999;Won et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Role of γ-aminobutyric acid B (GABAB) receptors in the regulation of kainic acid-induced cell death in mouse hippocampus

Lee

Seo²,

Choi³

et al. 2005

Exp Mol Med

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“…5,25,28 One catastrophic consequence of kainate treatment is widespread neuronal loss in limbic structures, including the hippocampal formation, neocortex, amygdala and selected thalamic areas. 4,[37][38][39] A number of studies has been performed to outline the neuronal events underlying kainate-induced seizure and neurodegeneration. The central effect of kainate appears to propagate through an increase in the release of glutamate and aspartate after activation of presynaptic kainate receptors, depolarization after activation of postsynaptic a-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)/kainate receptors, and the secondary activation of N-methyl-d-aspartate (NMDA) receptors.…”

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confidence: 99%