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Adenosine Involvement in Kindled Seizures

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Kindling 4

Part of the book series: Advances in Behavioral Biology ((ABBI,volume 37))

Abstract

Our interests have been focused on determining the role of adenosine in the development and maintenance of kindled seizures. The results from our studies, and those of others now indicate that adenosine may have a role in terminating ongoing seizure activity and may play a principal role in the development and expression of postictal events (i.e., EEG depression, spiking, refractory period). If adenosine contributes to seizure termination, it probably also serves to limit the generalization of seizures and thus the rate of kindling. If so, its role in kindling may be even more general than indicated by current available data. Of course, no single neurotransmitter or neuromodulator is likely to be solely responsible for the kindling phenomenon. In fact, several other neurotransmitters and neuromodulators are known to influence kindling and are undoubtedly involved. These include norepinephrine, acetylcholine, glutamate, GABA and probably others as well. Studies describing these systems are well represented by several papers in this volume. However, this review is focused only on adenosine, and specifically its possible role in kindling and kindling related phenomena (i.e., postictal depression, spiking).

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Author information

Authors and Affiliations

  1. Department of Psychology, Wayne State Univ., Detroit, MI, USA

    Robert F. Berman & Carl R. Lupica

  2. CIBA Geigy Corp., Summit, N.J., USA

    Michael F. Jarvis

Authors
  1. Robert F. Berman
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  2. Michael F. Jarvis
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  3. Carl R. Lupica
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Editors and Affiliations

  1. Neurosciences and Neurology, University of British Columbia, Vancouver, British Columbia, Canada

    Juhn A. Wada

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© 1990 Plenum Press, New York

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Berman, R.F., Jarvis, M.F., Lupica, C.R. (1990). Adenosine Involvement in Kindled Seizures. In: Wada, J.A. (eds) Kindling 4. Advances in Behavioral Biology, vol 37. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5796-4_31

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  • DOI: https://doi.org/10.1007/978-1-4684-5796-4_31

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4684-5798-8

  • Online ISBN: 978-1-4684-5796-4

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