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Genetic Predisposition and Kindling Susceptibility in Primates

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Kindling 5

Part of the book series: Advances in Behavioral Biology ((ABBI,volume 48))

Abstract

Among patients with temporal lobe epilepsy with a focus in identical anatomical locations, some patients have non-convulsive seizures exclusively, even when medication is withdrawn, while others begin with generalized convulsive seizures which readily recur when medication is reduced. Between these two extremes, there are those patients who display partial motor seizure without ever developing secondary generalization. The reason for such differences is not known. A less favorable prognosis has been suggested for those partial epilepsy patients with generalized seizures than for those without14,26,27. Furthermore, convulsive evolution in partial seizure is reported to be the major factor for a serious morbidity in status epilepticus6. An understanding of the mechanisms underlying convulsive evolution and its bilateralization/generalization is important since once they are defined, it may be possible to modify them for therapeutic or prophylactic purposes. However, due to the complexity and diversity of both etiologic and genetic factors in human epilepsy little progress has been made in our understanding, which is largely dependent on studies in animal models, of the underlying mechanisms. One of these models, kindling, has proved to be an ideal one for partial onset secondarily generalized seizure28. In this model, we have become accustomed to assessing the degree of kindling susceptibility by the speed with which convulsive development and its bilateralization/generalization occur. In general, once a day amygdaloid (AM) stimulation results in secondarily generalized convulsion in about two weeks in rodents, four weeks in cats, and 6–10 months in rhesus monkeys. Some strain difference has been noted within the same species as to the kindling rate24,46. In our laboratory we also noted, for example, that black hooded rats tend to kindle faster than Wister rats. Indeed, the potential contribution of genetic susceptibility has been studied by subjecting strains of mice17, gerbils2 and audiogenic rats to kindling4 assessing resultant evidence of interaction between kindling and intrinsic seizure predisposition.

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Authors and Affiliations

  1. Divisions of Neurosciences and Neurology, The University of British Columbia, Vancouver, British Columbia, Canada, V6T 2A1

    Juhn A. Wada

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  1. Juhn A. Wada
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Editors and Affiliations

  1. University of Saskatchewan, Saskatoon, Saskatchewan, Canada

    Michael E. Corcoran

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

    Solomon L. Moshé

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Wada, J.A. (1998). Genetic Predisposition and Kindling Susceptibility in Primates. In: Corcoran, M.E., Moshé, S.L. (eds) Kindling 5. Advances in Behavioral Biology, vol 48. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5375-5_1

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  • DOI: https://doi.org/10.1007/978-1-4615-5375-5_1

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-7453-4

  • Online ISBN: 978-1-4615-5375-5

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