Titlebook: Animal Models of Epilepsy; Methods and Innovati Scott C. Baraban Book 2009 The Editor(s) (if applicable) and The Author(s), under exclusive

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Val Roseg: A High Alpine Catchment,hat seizures elicited by acute convulsant treatment (i.e., pentylenetetrazole, PTZ) or knockdown of zebrafish homologs for human genetic epilepsy disorders (i.e., tuberous sclerosis complex, TSC) reliably evoke seizures in developing zebrafish. Using tectal or forebrain recordings, we also show that

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https://doi.org/10.1007/978-94-009-5524-0many neurological aspects of TSC. In this chapter I will review the clinical manifestations of TSC, molecular roles of the TSC genes, and current animal models of TSC. These and future models should facilitate the development of new and exciting discoveries that will have a meaningful impact on live

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W. G. Beeftink,J. Rozema,A. H. L. Huiskes of BFNC has helped solidify the link between attenuated . . function and increased seizure susceptibility that results from . and . mutations. The mouse models described here have all significantly contributed to our understanding of how mutations in these genes might precipitate human epilepsy and

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https://doi.org/10.1007/978-94-009-5524-0loss of specific subtypes of interneurons. Furthermore, electrophysiological studies have demonstrated that dentate gyrus granule cells from epileptic patients exhibit a functional reduction in inhibitory synaptic transmission (4). These clinical findings are consistent with extensive work in pharma

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C. Ferrari,R. Gerdol,F. Piccolihe conventional means of recording epileptiform events has always been, and likely will continue to be, electrophysiological, but a careful calibration of imaging signals with respect to electrophysiological recordings can extend our data set immeasurably, providing new insights into old problems.

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https://doi.org/10.3920/978-90-8686-744-8electrographic and behavioral seizure activity induced by peripheral kainic acid administration, prevents seizure-induced cell damage, and attenuates the seizure threshold in previously kindled animals. For NPY, AAV vector-mediated expression of prepro-neuropeptide Y delays seizure onset and increas

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Tick – , interactions: burden or benefit? their role in epileptogenesis or associated cognitive dysfunction. Other research on neural stem or progenitor cells suggest that cell grafts may offer a strategy to repair epileptogenic damage or to deliver anticonvulsant treatments. Thus, both manipulating endogenous neural progenitors and neural