Kainic acid seizures in the rat

Sperk, Günther

doi:10.1016/0301-0082(94)90019-1

Cited by 662 publications

(367 citation statements)

References 340 publications

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“…Seizure severity was graded according to a modified Racine scale. 4,14 Fifteen minutes after kainate injection, the mice were injected intraperitoneally with a combination of [1-13 C]glucose (543 mg/kg) and [1,[2][3][4][5][6][7][8][9][10][11][12][13] C]acetate (504 mg/kg) and after another 15 minutes, the brains of the mice were subjected to microwave fixation at 4 kW for 1.7 seconds (model GA5013, Gerling Applied Engineering, Modesto, CA, USA). This is the most humane euthanization method instantly inactivating proteins in the brain.…”

Section: Metabolic Studiesmentioning

confidence: 99%

“…If [4,[5][6][7][8][9][10][11][12][13] C]a-ketoglutarate remains in the astrocytic TCA cycle for further metabolism via this pathway, it will, after condensation with unlabeled acetyl CoA, give rise to [3-13 C]-and [1,2-13 C]a-ketoglutarate in the subsequent turn, which may give rise to glutamate and glutamine displaying the same labeling patterns. Based on the distinct 13 C labeling in glutamine after the first and second turn of TCA cycle metabolism, a number indicative of astrocytic TCA cycle activity can be calculated by relating the amount of isotopomers generated in the second turn of TCA cycle metabolism to the amount of that generated in the first turn, i.e., ( [1,[2][3][4][5][6][7][8][9][10][11][12][13] …”

Section: Nuclear Magnetic Resonance Spectroscopymentioning

confidence: 99%

“…In glutamatergic neurons, this [4,[5][6][7][8][9][10][11][12][13] C]glutamate may be released upon depolarization. Otherwise, [4,[5][6][7][8][9][10][11][12][13] C]glutamate may be converted to [4,[5][6][7][8][9][10][11][12][13] C]a-ketoglutarate for further TCA cycle metabolism or may in GABAergic neurons be converted to [1,[2][3][4][5][6][7][8][9][10][11][12][13] C]GABA. It should be noted that the largest pool of glutamate is situated in the glutamatergic neurons and the [4,[5][6][7][8][9][10]…”

Section: Nuclear Magnetic Resonance Spectroscopymentioning

confidence: 99%

“…The convulsive effects of kainate are time and concentration dependent [3][4][5] and the seizure propagation reflects the etiology of temporal lobe epilepsy observed in patients, i.e., it involves an initial precipitating injury followed by a latent phase before the chronic phase characterized by spontaneous seizures ensues. 6 Metabolic changes in the cerebral cortex 24 hours after a systemic injection of a convulsive dose of kainate have been demonstrated to mainly involve the astrocyte compartment.…”

Section: Introductionmentioning

confidence: 99%

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A Subconvulsive Dose of Kainate Selectively Compromises Astrocytic Metabolism in the Mouse Brain In Vivo

Walls

Eyjolfsson

Schousboe

et al. 2014

J Cereb Blood Flow Metab

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Despite the well-established use of kainate as a model for seizure activity and temporal lobe epilepsy, most studies have been performed at doses giving rise to general limbic seizures and have mainly focused on neuronal function. Little is known about the effect of lower doses of kainate on cerebral metabolism and particularly that associated with astrocytes. We investigated astrocytic and neuronal metabolism in the cerebral cortex of adult mice after treatment with saline (controls), a subconvulsive or a mildly convulsive dose of kainate. A combination of [1,2-13 C]acetate and [1-13 C]glucose was injected and subsequent nuclear magnetic resonance spectroscopy of cortical extracts was employed to distinctively map astrocytic and neuronal metabolism. The subconvulsive dose of kainate led to an instantaneous increase in the cortical lactate content, a subsequent reduction in the amount of [4,[5][6][7][8][9][10][11][12][13] C]glutamine and an increase in the calculated astrocytic TCA cycle activity. In contrast, the convulsive dose led to decrements in the cortical content and 13 C labeling of glutamate, glutamine, GABA, and aspartate. Evidence is provided that astrocytic metabolism is affected by a subconvulsive dose of kainate, whereas a higher dose is required to affect neuronal metabolism. The cerebral glycogen content was dose-dependently reduced by kainate supporting a role for glycogen during seizure activity.

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Section: Metabolic Studiesmentioning

confidence: 99%

Section: Nuclear Magnetic Resonance Spectroscopymentioning

confidence: 99%

Section: Nuclear Magnetic Resonance Spectroscopymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

A Subconvulsive Dose of Kainate Selectively Compromises Astrocytic Metabolism in the Mouse Brain In Vivo

Walls

Eyjolfsson

Schousboe

et al. 2014

J Cereb Blood Flow Metab

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“…While a number of experimental animal models have been developed to help elucidate the pathophysiology of this condition (reviewed in Löscher, 1997Löscher, , 2002Coulter et al, 2002;Morimoto et al, 2004), one of the most widely used animal models of temporal lobe epilepsy (Sperk, 1994) involves the systemic administration of chemoconvulsants, such as kainic acid (KA), a potent agonist of the AMPA/kainate class of glutamate receptors. Systemic and intracerebral administration of kainic acid (KA) initially induces a characterized pattern of seizure activity (Coyle, 1983) that lasts for hours, followed by a latent seizure-free period of weeks, preceding the development of spontaneous recurrent focal seizures that begin between 3-4 weeks (Brandt et al, 2003).…”

Section: Nih-pa Author Manuscriptmentioning

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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Secretoneurin: A marker in rat hippocampal pathways

et al. 1997

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Secretoneurin is a 33-amino acid peptide, generated in brain by proteolytic processing of secretogranin II. The distribution of secretoneurin-like immunoreactivity and secretogranin II mRNA was investigated in the hippocampus of the rat. Secretogranin II mRNA was found in high concentrations throughout the granule cell and pyramidal cell layers and in many local neurons, notably in the hilus of the dentate gyrus. The general distributional pattern of secretoneurin-like immunoreactivity was characterized by a prominent staining in the area of the terminal field of mossy fibers with an obvious staining in the infrapyramidal area of CA3 and a strongly immunopositive band in the inner third of the molecular layer of the dentate gyrus. Lesions of the granule cells by local injection of colchicine significantly reduced secretoneurin-like immunoreactivity in the terminal field of mossy fibers, but not in the inner molecular layer of the dentate gyrus. On the other hand, destruction of interneurons of the dentate gyrus (mossy cells and certain gamma-aminobutyricacid-ergic interneurons) by kainic acid-induced seizures was associated with a reduction of secretoneurin-like immunoreactivity in the inner molecular layer of the dentate gyrus. However, 30 days after kainic acid-induced seizures, a strongly secretoneurin-immunoreactive band reappeared in this area, which at this late time point is due to sprouting of mossy fibers collaterals. Our experiments suggest a widespread distribution of secretoneurin-like immunoreactivity in neurons of the hippocampal formation with a preferential localization in excitatory pathways including associational/commissural fibers originating from secretoneurin-containing mossy cells.

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Kainic acid seizures in the rat

Cited by 662 publications

References 340 publications

A Subconvulsive Dose of Kainate Selectively Compromises Astrocytic Metabolism in the Mouse Brain In Vivo

A Subconvulsive Dose of Kainate Selectively Compromises Astrocytic Metabolism in the Mouse Brain In Vivo

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

Secretoneurin: A marker in rat hippocampal pathways

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