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Kainate and Temporal Lobe Epilepsies: 3 decades of progress.


Ben-Ari Y1.


Jasper's Basic Mechanisms of the Epilepsies [Internet]. 4th edition. Bethesda (MD): National Center for Biotechnology Information (US); 2012.

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INMED, INSERM U 901, Scientific Campus of luminy, 163, route de luminy, Marseilles, France


In the early 1980s, kainate was isolated from sea weeds and its excessive excitatory actions on central neurons identified. This led to a flurry of studies that have provided most of the concepts now considered instrumental in TLE, including mechanisms of cell loss, failure of GABAergic inhibition, sprouting of fibres, and formation of aberrant synapses - that in turn reduce the threshold for further seizures. Recent studies have identified kainatergic synapses in the brain and showed that as with other natural molecules- e.g., opiates and endorphins -these synapses play an important role in brain function. An understanding of these synapses provides valuable insight as to how the brain operates in health and disease. “Kainatergic” synapses –as they can now be called - have unique features and are enriched in neurons that are also vulnerable to seizures and to their sequel, thereby bridging the gap between the actions of an exogenous molecule and its physiological and pathological actions. Here, I review the history of this transmitter pathway, emphasizing the importance of studying in parallel the physiological and pathological actions of biologically active molecules, and the importance of reactive plasticity that should be taken into account in the development of efficient antiepileptic agents. I also discuss fundamental issues related to how seizures are generated, how they produce long term effects in both the developing and adult brain.

Copyright © 2012, Michael A Rogawski, Antonio V Delgado-Escueta, Jeffrey L Noebels, Massimo Avoli and Richard W Olsen.

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