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Neurotrophins and Kindling Epileptogenesis

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Kindling 5

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

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Abstract

Molecular and cellular mechanisms underlying the development of abnormal excitability in kindling and human epilepsy are poorly understood39. One major working hypothesis is that maintenance of the epileptic syndrome is caused by structural rearrangements occurring during epileptogenesis, e. g., sprouting of mossy fibres in the supragranular layer of the dentate gyrus and the infrapyramidal layer of CA3. Such plastic responses could be triggered by trophic factors, the synthesis of which may be influenced by seizure activity. During recent years much interest in this regard has been focussed on the neurotrophin family of trophic molecules, nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3), and their high-affinity receptors trkA, trkB and trkC35.

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Lindvall, O., Kokaia, Z., Elmér, E., Ferencz, I., Bengzon, J., Kokaia, M. (1998). Neurotrophins and Kindling Epileptogenesis. 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_22

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  • DOI: https://doi.org/10.1007/978-1-4615-5375-5_22

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