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一个控制甲基-β-咔啉-3-羧酸盐(β-CCM)诱发癫痫的多基因系统的证据。

Evidence for a multigenic system controlling methyl-beta-carboline-3-carboxylate (beta-CCM)-induced seizures.

作者信息

Martin B, Marchaland C, Chapouthier G, Motta R

机构信息

URA 1294-CNRS, UFR Biomédicale Paris V, France.

出版信息

Behav Genet. 1994 May;24(3):285-97. doi: 10.1007/BF01067195.

DOI:10.1007/BF01067195
PMID:7945158
Abstract

beta-CCM is a beta-carboline known to have properties opposite to those of benzodiazepines. Our approach was to analyze, in mice, the genetic mechanisms involved in beta-CCM-induced myoclonic seizures using recombinant congenic strains and F1 hybrids issued from these strains. Our aim was to define the extent of the multigenic character of beta-CCM-induced myoclonic seizures, while also evaluating the distribution of the strength of the genes implicated in this trait. The results show that the control of reactivity to beta-CCM is multigenic with notable epistatic involvement.

摘要

β-CCM是一种已知具有与苯二氮䓬类药物相反特性的β-咔啉。我们的方法是在小鼠中,使用重组近交系和由这些品系产生的F1杂种,分析β-CCM诱导的肌阵挛性癫痫发作所涉及的遗传机制。我们的目的是确定β-CCM诱导的肌阵挛性癫痫发作的多基因特征程度,同时评估与该性状相关基因的强度分布。结果表明,对β-CCM反应性的控制是多基因的,且存在显著的上位性参与。

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Mamm Genome. 1997 Mar;8(3):200-8. doi: 10.1007/s003359900389.
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