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Pentylenetetrazol-Induced Kindling as a Model of Absence and Convulsive forms of Epilepsy

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Kindling 6

Part of the book series: Advances in Behavioral Biology ((ABBI,volume 55))

Abstract

The electrically and chemically induced kindling is a model of human epilepsy. Whereas the electrical kindling is regarded as a model of complex partial epilepsy,1,2,3 the chemical kindling6,7 is a model of primary generalized epilepsy.5 Although pentylenetetrazol (PTZ) kindling has often been used to explore the mechanisms of seizure genesis and neurobehavioral and neurophysiological consequences of seizures, limited attention was paid to the contribution of this model in the mechanisms of the generalized nonconvulsive epilepsy-absence model.8–17 Meanwhile, complex evaluation of this model should be performed as far as divergent and even opposite mechanisms of epileptogenesis might be suspected in the course of generalized absence and convulsive stages of PTZ-kindling. Thus, first one is characterized by absence-like manifestations (spike-wave discharges (SWD)-bursts) and is supported by hyperexcitable state of all cortical neurons, including inhibitory ones, while receptors of GABA are preserved and their hyperactivation is resulted in typical generalized spike-wave generation.18–19 Further increasing of epileptogenic stimuli is followed by collapse of GABA control, and precipitation of generalized seizures as a result.

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Author information

Authors and Affiliations

  1. Odessa State Medical University, Odessa, Ukraine, 65026

    Leonid S. Godlevsky

Authors
  1. Alexey A. Shandra
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  2. Leonid S. Godlevsky
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Editor information

Editors and Affiliations

  1. University of Saskatchewan, Saskatoon, Saskatchewan, Canada

    Michael E. Corcoran

  2. Albert Einstein College of Medicine, Yeshiva University, Bronx, New York, USA

    Solomon L. Moshé

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Shandra, A.A., Godlevsky, L.S. (2005). Pentylenetetrazol-Induced Kindling as a Model of Absence and Convulsive forms of Epilepsy. In: Corcoran, M.E., Moshé, S.L. (eds) Kindling 6. Advances in Behavioral Biology, vol 55. Springer, Boston, MA. https://doi.org/10.1007/0-387-26144-3_6

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