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Genetic threshold hypothesis of neocortical spike‐and‐wave discharges in the rat: An animal model of petit mal epilepsy

Genetic threshold hypothesis of neocortical spike‐and‐wave discharges in the rat: An animal model... Neocortical high‐voltage spike‐and‐wave discharges (HVS) in the rat are an animal model of petit mal epilepsy. Genetic analysis of total duration of HVS (s/12 hr) in reciprocal F1 and F2 hybrids of F344 and BN rats indicated that the phenotypic variability of HVS cannot be explained by a simple, monogenic Mendelian model. Biometrical analysis suggested the presence of additive, dominance, and sex‐linked‐epistatic effects, buffering maternal influence, and heterosis. High correlation was observed between average duration (s/episode) and frequency of occurrence of spike‐and‐wave episodes (n/12 hr) in parental and segregating generations, indicating that common genes affect both duration and frequency of the spike‐and‐wave pattern. We propose that both genetic and developmental‐environmental factors control an underlying quantitative variable, which, above a certain threshold level, precipitates HVS discharges. These findings, together with the recent availability of rat DNA markers for total genome mapping, pave the way to the identification of genes that control the susceptibility of the brain to spike‐and‐wave discharges. © 1995 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png American Journal of Medical Genetics Part A Wiley

Genetic threshold hypothesis of neocortical spike‐and‐wave discharges in the rat: An animal model of petit mal epilepsy

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References (50)

Publisher
Wiley
Copyright
Copyright © 1995 Wiley Subscription Services, Inc., A Wiley Company
ISSN
1552-4825
eISSN
1552-4833
DOI
10.1002/ajmg.1320600111
pmid
7485236
Publisher site
See Article on Publisher Site

Abstract

Neocortical high‐voltage spike‐and‐wave discharges (HVS) in the rat are an animal model of petit mal epilepsy. Genetic analysis of total duration of HVS (s/12 hr) in reciprocal F1 and F2 hybrids of F344 and BN rats indicated that the phenotypic variability of HVS cannot be explained by a simple, monogenic Mendelian model. Biometrical analysis suggested the presence of additive, dominance, and sex‐linked‐epistatic effects, buffering maternal influence, and heterosis. High correlation was observed between average duration (s/episode) and frequency of occurrence of spike‐and‐wave episodes (n/12 hr) in parental and segregating generations, indicating that common genes affect both duration and frequency of the spike‐and‐wave pattern. We propose that both genetic and developmental‐environmental factors control an underlying quantitative variable, which, above a certain threshold level, precipitates HVS discharges. These findings, together with the recent availability of rat DNA markers for total genome mapping, pave the way to the identification of genes that control the susceptibility of the brain to spike‐and‐wave discharges. © 1995 Wiley‐Liss, Inc.

Journal

American Journal of Medical Genetics Part AWiley

Published: Mar 27, 1997

Keywords: ; ; ; ;

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