A mutation causing increased KATP channel activity leads to reduced anxiety in mice

被引：14

作者：

Lahmann, Carolina ^{[1
]}

Clark, Rebecca H. ^{[1
]}

Iberl, Michaela ^{[1
]}

Ashcroft, Frances M. ^{[1
]}

机构：

[1] Univ Oxford, Dept Physiol Anat & Genet, Henry Wellcome Ctr Gene Funct, Oxford OX1 3PT, England

来源：

PHYSIOLOGY & BEHAVIOR | 2014年 / 129卷

基金：

英国惠康基金;

关键词：

K-ATP channels; Neonatal diabetes; Anxiety; Hyperactivity; ACTIVATING MUTATIONS; SUBUNIT KIR6.2; NERVOUS-SYSTEM; HIPPOCAMPUS; HOMEOSTASIS; EXPRESSION; GLYBURIDE; INSULIN; LACKING;

D O I：

10.1016/j.physbeh.2014.02.031

中图分类号：

B84 [心理学];

学科分类号：

04 ; 0402 ;

摘要：

Activating mutations in the Kir6.2 (KCNJ11) subunit of the ATP-sensitive potassium channel cause neonatal diabetes. Many patients also suffer from neurological complications. By using mice carrying a human Kir6.2 mutation (Val(59) to Met(59); nV59M mice) targeted to neurones, we show that these mutations also result in altered anxiety behaviour. The light/dark box, successive alleys and elevated plus maze tasks revealed that nV59M mice have reduced anxiety related responses. Additionally, nV59M mice displayed enhanced basal locomotor activity and exploratory behaviour, as assessed by the low anxiety open-field test. These findings, in combination with previously reported hyperactivity of nV59M mice, appear to correlate with the increased impulsivity and inattentiveness reported in iDEND/DEND patients. (C) 2014 Published by Elsevier Inc.

引用

页码：79 / 84

页数：6

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