Literature DB >> 24184743

The kainic acid model of temporal lobe epilepsy.

Maxime Lévesque1, Massimo Avoli.   

Abstract

The kainic acid model of temporal lobe epilepsy has greatly contributed to the understanding of the molecular, cellular and pharmacological mechanisms underlying epileptogenesis and ictogenesis. This model presents with neuropathological and electroencephalographic features that are seen in patients with temporal lobe epilepsy. It is also characterized by a latent period that follows the initial precipitating injury (i.e., status epilepticus) until the appearance of recurrent seizures, as observed in the human condition. Finally, the kainic acid model can be reproduced in a variety of species using either systemic, intrahippocampal or intra-amygdaloid administrations. In this review, we describe the various methodological procedures and evaluate their differences with respect to the behavioral, electroencephalographic and neuropathological correlates. In addition, we compare the kainic acid model with other animal models of temporal lobe epilepsy such as the pilocarpine and the kindling model. We conclude that the kainic acid model is a reliable tool for understanding temporal lobe epilepsy, provided that the differences existing between methodological procedures are taken into account.
Copyright © 2013 Elsevier Ltd. All rights reserved.

Entities:  

Keywords:  Animal models of temporal lobe epilepsy; Intracerebral administration; Kainic acid; Systemic administration

Mesh:

Substances:

Year:  2013        PMID: 24184743      PMCID: PMC4878897          DOI: 10.1016/j.neubiorev.2013.10.011

Source DB:  PubMed          Journal:  Neurosci Biobehav Rev        ISSN: 0149-7634            Impact factor:   8.989


  188 in total

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3.  Blood-brain barrier dysfunctions following systemic injection of kainic acid in the rat.

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4.  Altered synaptic physiology and reduced susceptibility to kainate-induced seizures in GluR6-deficient mice.

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Journal:  Nature       Date:  1998-04-09       Impact factor: 49.962

5.  Altered hippocampal kainate-receptor mRNA levels in temporal lobe epilepsy patients.

Authors:  G W Mathern; J K Pretorius; H I Kornblum; D Mendoza; A Lozada; J P Leite; L Chimelli; D E Born; I Fried; A C Sakamoto; J A Assirati; W J Peacock; G A Ojemann; P D Adelson
Journal:  Neurobiol Dis       Date:  1998-09       Impact factor: 5.996

6.  Cerebral metabolic response to systemic kainic acid: 14-C-deoxyglucose studies.

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7.  AIDA, a class I metabotropic glutamate-receptor antagonist limits kainate-induced hippocampal dysfunction.

Authors:  Johanne Renaud; Martine Emond; Sébastien Meilleur; Caterina Psarropoulou; Lionel Carmant
Journal:  Epilepsia       Date:  2002-11       Impact factor: 5.864

8.  Brain-state- and cell-type-specific firing of hippocampal interneurons in vivo.

Authors:  Thomas Klausberger; Peter J Magill; László F Márton; J David B Roberts; Philip M Cobden; György Buzsáki; Peter Somogyi
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9.  Intra-amygdaloid injections of kainic acid: regional metabolic changes and their relation to the pathological alterations.

Authors:  E Tremblay; O P Ottersen; C Rovira; Y Ben-Ari
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  134 in total

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5.  Rapid throughput analysis demonstrates that chemicals with distinct seizurogenic mechanisms differentially alter Ca2+ dynamics in networks formed by hippocampal neurons in culture.

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7.  The Pilocarpine Model of Temporal Lobe Epilepsy and EEG Monitoring Using Radiotelemetry System in Mice.

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Review 8.  Animal models of temporal lobe epilepsy following systemic chemoconvulsant administration.

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