BEHAVIORAL AND MOLECULAR CHANGES IN THE MOUSE IN RESPONSE TO PRENATAL EXPOSURE TO THE ANTI-EPILEPTIC DRUG VALPROIC ACID

被引：169

作者：

Roullet, F. I. ^{[1
,2
]}

Wollaston, L. ^{[1
,2
]}

Decatanzaro, D. ^{[3
]}

Foster, J. A. ^{[1
,2
]}

机构：

[1] McMaster Univ, Brain Body Inst, Hamilton, ON L8N 4A6, Canada

[2] McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON L8N 4A6, Canada

[3] McMaster Univ, Dept Psychol Neurosci & Behav, Hamilton, ON L8N 4A6, Canada

来源：

NEUROSCIENCE | 2010年 / 170卷 / 02期

基金：

加拿大自然科学与工程研究理事会;

关键词：

valproic acid; social behavior; brain derived neurotrophic factor; gene expression; in situ hybridization; AUTISM SPECTRUM DISORDERS; ANIMAL-MODEL; NEUROTROPHIC FACTOR; MENTAL-RETARDATION; MESSENGER-RNA; RODENT MODEL; RAT-BRAIN; CHILDREN; BDNF; MICE;

D O I：

10.1016/j.neuroscience.2010.06.069

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Experiments in rodents have indicated that maternal valproic acid (VPA) exposure has permanent adverse effects upon neurological and behavioral development. In humans, prenatal exposure to VPA can induce fetal valproate syndrome, which has been associated with autism. The present study examined mouse pups exposed in utero to VPA, measuring physical development, olfactory discrimination, and social behavior as well as expression of plasticity-related genes, brain derived neurotrophic factor (BDNF) and NMDA receptor subunits NR2A and NR2B. VPA-exposed mice showed delayed physical development, impaired olfactory discrimination, and dysfunctional pre-weaning social behavior. In situ hybridization experiments revealed lower cortical expression of BDNF mRNA in VPA animals. These results support the validity of the VPA mouse model for human autism and suggest that alterations in plasticity-related genes may contribute to the behavioral phenotype. (C) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.

引用

页码：514 / 522

页数：9

共 79 条

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