Elsevier

Life Sciences

Volume 29, Issue 20, 16 November 1981, Pages 2031-2042
Life Sciences

Minireview
Kainic acid as a tool for the study of temporal lobe epilepsy

https://doi.org/10.1016/0024-3205(81)90659-7Get rights and content

Abstract

Temporal lobe epilepsy (limbic epilepsy, complex partial epilepsy, psychomotor epilepsy) is the most devastating form of epilepsy commonly encountered in the adult population. The attacks involve loss of consciousness, thus limiting performance of normal functions and exposing the individual to bodily injury. Moreover, long-standing or pharmacologically intractable temporal lobe epilepsy is frequently associated with the loss of neurons from the hippocampus and other brain regions (Ammon's horn sclerosis (AHS)). Unfortunately, pharmacologically intractable cases are rather common, owing to the relatively low efficacy against this condition of the available anticonvulsants. Progress in the understanding and treatment of temporal lobe epilepsy would be greatly facilitated by the availability of an animal model which reproduced the behavioral, electrographic and pathological features of this condition. Here I review evidence which indicates that the kainic acid (KA)-treated rat possesses many of the features required of such a model.

References (98)

  • H. Shinozaki et al.

    Brain Res.

    (1970)
  • J.W. Olney et al.

    Brain Res.

    (1974)
  • Y. Ben-Ari et al.

    Neuroscience

    (1980)
  • J.O. McNamara et al.

    Prog. Neurobiol.

    (1980)
  • R. Schwarcz et al.

    Eur. J. Pharmacol.

    (1978)
  • Y. Ben-Ari et al.

    Brain Res.

    (1980)
  • R.C. Collins et al.

    Life Sci.

    (1980)
  • R. Zaczek et al.

    Eur. J. Pharmacol.

    (1978)
  • R. Zaczek et al.

    Neuropharmacology

    (1981)
  • T.A. Fuller et al.

    Life Sci.

    (1979)
  • J.M. Liebman et al.

    Life Sci.

    (1980)
  • E.D. London et al.

    Eur. J. Pharmacol.

    (1979)
  • P.A. Schwartzkroin et al.

    Brain Res.

    (1978)
  • J.W. Olney et al.

    Brain Res.

    (1980)
  • R. Schwarcz et al.

    Neuropharmacology

    (1978)
  • C. de Montigny et al.

    Neuroscience

    (1980)
  • C. Kohler et al.

    Brain Res.

    (1979)
  • R. Schwarcz et al.

    Neurosci. Lett.

    (1980)
  • Y. Ben-Ari et al.

    Brain Res.

    (1979)
  • J.E. Schwob et al.

    Neuroscience

    (1980)
  • S.M. Wuerthele et al.

    Brain Res.

    (1978)
  • U. Scherer-Singler et al.

    Life Sci.

    (1979)
  • R.A. Mesher et al.

    Brain Res.

    (1980)
  • J.W. Olney et al.

    Brain Res.

    (1979)
  • A.B. Butler et al.

    Exp. Neurol.

    (1976)
  • I. Fried et al.

    Soc. Neurosci. Abstr.

    (1979)
  • W.J. Brown

    Epilepsy: Its Phenomena in Man

  • M.A. Falconer

    Lancet

    (1974)
  • J.V. Nadler et al.

    Brain Res.

    (1980)
  • K. Biziere et al.

    Neurosci. Lett.

    (1978)
  • C. Kohler et al.

    Neurosci. Lett.

    (1978)
  • D. Malthe-Sørenssen et al.

    Brain Res.

    (1980)
  • E.G. McGeer et al.

    Brain Res.

    (1978)
  • P. Streit et al.

    Brain Res.

    (1980)
  • H. McLennan

    Neurosci. Lett.

    (1980)
  • K. Biziere et al.

    Neuropharmacology

    (1979)
  • M. Pisa et al.

    Brain Res.

    (1980)
  • J.W. Olney et al.

    Soc. Neurosci. Abstr.

    (1975)
  • J.V. Nadler et al.

    Nature

    (1978)
  • E.G. McGeer et al.

    Kainic Acid Ass a Tool in Neurobiology

    (1978)
  • J.V. Nadler

    Life Sci.

    (1978)
  • J.T. Coyle et al.

    Neurosciences Research Program Bulletin

    (1981)
  • P.M. Lenique et al.

    Psychopharmacology

    (1979)
  • J.W. Olney
  • R. Racine

    Neurosurgery

    (1978)
  • M.F. Nelson et al.

    J. Pharmacol. Exp. Ther.

    (1980)
  • J.V. Nadler et al.

    Kainic Acid As a Tool in Neurobiology

  • Z. Kleinrok et al.

    Naunyn-Schmieds. Archs. Pharmacol.

    (1980)
  • T. Lanthorn et al.

    Life Sci.

    (1978)
  • Cited by (533)

    • Glutamate receptor endocytosis and signaling in neurological conditions

      2023, Progress in Molecular Biology and Translational Science
    • Involvement of monocarboxylate transporters in the cross-tolerance between epilepsy and cerebral infarction: A promising choice towards new treatments

      2019, Neuroscience Letters
      Citation Excerpt :

      After 15 min of MCAO, reperfusion was performed by removing the filament. A glutamate analogue KA protocol was used to induce epilectic seizures in rats, consisting of intraperitoneal (i.p.) injections with KA (15 mg/kg) to evoke behavioral seizures known resembling human temporal lobe epilepsy [13]. The a-cyano-4-hydroxycinnamate (CHC; Sigma-Aldrich, St. Louis, MO, USA; 90 mg/kg) which is a specific covalent inhibitor of mitochondrial lactate and pyruvate transport [14] was intraperitoneal injected 4 h before KA injection.

    View all citing articles on Scopus
    View full text