Early embryonic ethanol exposure impairs shoaling and the dopaminergic and serotoninergic systems in adult zebrafish

被引:115
作者
Buske, Christine [2 ]
Gerlai, Robert [1 ,2 ]
机构
[1] Univ Toronto, Dept Psychol, Mississauga, ON L5L 1C6, Canada
[2] Univ Toronto, Dept Cell & Syst Biol, Mississauga, ON L5L 1C6, Canada
关键词
Zebrafish; Fetal alcohol syndrome; Dopamine; Serotonin; Social behavior; Ethanol; DANIO-RERIO; SCHOOLING BEHAVIOR; ALCOHOL EXPOSURE; FISH; MOUSE; MODEL;
D O I
10.1016/j.ntt.2011.05.009
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
Fetal alcohol syndrome (FAS) is a devastating disorder accompanied by numerous morphological and behavioral abnormalities. Human FAS has been modeled in laboratory animals including the zebrafish. Recently, embryonic exposure to low doses of ethanol has been shown to impair behavior without any gross morphological alterations in zebrafish. The exposed zebrafish showed reduced responses to animated conspecific images. The effect of embryonic ethanol exposure, however, has not been investigated in a real shoal and the potential mechanisms underlying the behavioral impairment are also unknown. Here we show that a 2 h long immersion in 0.25% and 0.50% (vol/vol) alcohol at 24 h post fertilization significantly increases the distance among members of freely swimming groups of zebrafish when measured at 70 days post fertilization. We also show that this impaired behavior is accompanied by reduced levels of dopamine, DOPAC, serotonin and 5HIAA as quantified by HPLC from whole brain extracts. Our results demonstrate that even very low concentrations of alcohol applied for a short period of time during the development of zebrafish can impair behavior and brain function. We argue that the observed behavioral impairment is not likely to be due to altered performance capabilities, e.g. motor function or perception, but possibly to social behavior itself. We also argue that our neurochemical data represent the first step towards understanding the mechanisms of this abnormality in zebrafish, which may lead to better modeling of, and ultimately perhaps better therapies for human FAS. (C) 2011 Elsevier Inc. All rights reserved.
引用
收藏
页码:698 / 707
页数:10
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