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Ethanol promotes neuronal apoptosis by inhibiting phosphatidylserine accumulation.乙醇通过抑制磷脂酰丝氨酸积累来促进神经元凋亡。
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本文引用的文献

1
Unilateral whisker clipping exacerbates ethanol-induced social and somatosensory behavioral deficits in a sex- and age-dependent manner.单侧触须修剪会以性别和年龄依赖的方式加剧乙醇诱导的社交和躯体感觉行为缺陷。
Physiol Behav. 2015 Sep 1;148:166-75. doi: 10.1016/j.physbeh.2014.09.002. Epub 2014 Oct 2.
2
Effects of moderate prenatal ethanol exposure and age on social behavior, spatial response perseveration errors and motor behavior.孕期适度乙醇暴露及年龄对社交行为、空间反应持续性错误和运动行为的影响。
Behav Brain Res. 2014 Aug 1;269:44-54. doi: 10.1016/j.bbr.2014.04.029. Epub 2014 Apr 24.
3
Acute exposure to ethanol on gestational day 15 affects social motivation of female offspring.在妊娠第15天急性暴露于乙醇会影响雌性后代的社交动机。
Behav Brain Res. 2014 Mar 15;261:106-9. doi: 10.1016/j.bbr.2013.12.016. Epub 2013 Dec 16.
4
Sensory control of balance: a comparison of children with fetal alcohol spectrum disorders to children with typical development.平衡的感觉控制:胎儿酒精谱系障碍儿童与发育正常儿童的比较
J Popul Ther Clin Pharmacol. 2013;20(3):e212-28. Epub 2013 Sep 6.
5
Effects of ethanol on social approach and 50 kHz ultrasonic vocalization production in adolescent male Sprague-Dawley rats.乙醇对青春期雄性斯普拉格-道利大鼠社交接近行为和50千赫兹超声波发声的影响。
Dev Psychobiol. 2014 May;56(4):857-63. doi: 10.1002/dev.21143. Epub 2013 Sep 30.
6
Acute prenatal exposure to a moderate dose of valproic acid increases social behavior and alters gene expression in rats.孕期急性暴露于中等剂量丙戊酸会增加大鼠的社交行为并改变其基因表达。
Int J Dev Neurosci. 2013 Dec;31(8):740-50. doi: 10.1016/j.ijdevneu.2013.09.002. Epub 2013 Sep 19.
7
Sensory-motor deficits in children with fetal alcohol spectrum disorder assessed using a robotic virtual reality platform.使用机器人虚拟现实平台评估胎儿酒精谱系障碍儿童的感觉运动缺陷。
Alcohol Clin Exp Res. 2014 Jan;38(1):116-25. doi: 10.1111/acer.12225. Epub 2013 Aug 5.
8
Prenatal alcohol exposure results in long-term serotonin neuron deficits in female rats: modulatory role of ovarian steroids.产前酒精暴露导致雌性大鼠长期 5-羟色胺神经元缺失:卵巢类固醇的调节作用。
Alcohol Clin Exp Res. 2014 Jan;38(1):152-60. doi: 10.1111/acer.12224. Epub 2013 Aug 5.
9
Omega-3 fatty acids can reverse the long-term deficits in hippocampal synaptic plasticity caused by prenatal ethanol exposure.ω-3 脂肪酸可逆转产前乙醇暴露导致的海马突触可塑性的长期缺陷。
Neurosci Lett. 2013 Sep 13;551:7-11. doi: 10.1016/j.neulet.2013.05.051. Epub 2013 Jul 18.
10
Maternal touch moderates sex differences in juvenile social play behavior.母爱抚摸调节幼年社交玩耍行为的性别差异。
PLoS One. 2013;8(2):e57396. doi: 10.1371/journal.pone.0057396. Epub 2013 Feb 27.

二十二碳六烯酸可部分改善产前乙醇暴露所致的社会行为和超声发声缺陷。

Docosahexaenoic acid partially ameliorates deficits in social behavior and ultrasonic vocalizations caused by prenatal ethanol exposure.

作者信息

Wellmann Kristen A, George Finney, Brnouti Fares, Mooney Sandra M

机构信息

Department of Pediatrics, University of Maryland, Baltimore, MD 21201, United States.

Department of Pediatrics, University of Maryland, Baltimore, MD 21201, United States.

出版信息

Behav Brain Res. 2015 Jun 1;286:201-11. doi: 10.1016/j.bbr.2015.02.048. Epub 2015 Mar 5.

DOI:10.1016/j.bbr.2015.02.048
PMID:25746516
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4392387/
Abstract

Prenatal ethanol exposure disrupts social behavior in humans and rodents. One system particularly important for social behavior is the somatosensory system. Prenatal ethanol exposure alters the structure and function of this area. Docosahexaenoic acid (DHA), an omega 3 polyunsaturated fatty acid, is necessary for normal brain development and brains from ethanol-exposed animals are DHA deficient. Thus, we determined whether postnatal DHA supplementation ameliorated behavioral deficits induced by prenatal ethanol exposure. Timed pregnant Long-Evans rats were assigned to one of three groups: ad libitum access to an ethanol-containing liquid diet, pair fed an isocaloric isonutritive non-alcohol liquid diet, or ad libitum access to chow and water. Pups were assigned to one of two postnatal treatment groups; gavaged intragastrically once per day between postnatal day (P)11 and P20 with DHA (10 mg/kg in artificial rat milk) or artificial rat milk. A third group was left untreated. Isolation-induced ultrasonic vocalizations (iUSVs) were recorded on P14. Social behavior and play-induced USVs were tested on P28 or P42. Somatosensory performance was tested with a gap crossing test around P33 or on P42. Anxiety was tested on elevated plus maze around P35. Animals exposed to ethanol prenatally vocalized less, play fought less, and crossed a significantly shorter gap than control-treated animals. Administration of DHA ameliorated these ethanol-induced deficits such that the ethanol-exposed animals given DHA were no longer significantly different to control-treated animals. Thus, DHA administration may have therapeutic value to reverse some of ethanol's damaging effects.

摘要

产前乙醇暴露会破坏人类和啮齿动物的社交行为。对于社交行为特别重要的一个系统是体感系统。产前乙醇暴露会改变该区域的结构和功能。二十二碳六烯酸(DHA),一种ω-3多不饱和脂肪酸,是正常大脑发育所必需的,而乙醇暴露动物的大脑缺乏DHA。因此,我们确定产后补充DHA是否能改善产前乙醇暴露引起的行为缺陷。将定时怀孕的Long-Evans大鼠分为三组之一:自由摄取含乙醇的液体饮食、配对喂食等热量等营养的无酒精液体饮食,或自由摄取食物和水。幼崽被分配到两个产后治疗组之一;在出生后第(P)11天至P20天之间,每天一次通过灌胃给予DHA(在人工大鼠奶中为10mg/kg)或人工大鼠奶。第三组不进行治疗。在P14记录隔离诱导的超声波发声(iUSV)。在P28或P42测试社交行为和玩耍诱导的USV。在P33左右或P42用间隙穿越测试来测试体感性能。在P35左右在高架十字迷宫上测试焦虑。产前暴露于乙醇的动物发声较少,玩耍打斗较少,穿越的间隙明显比对照处理的动物短。给予DHA改善了这些乙醇诱导的缺陷,使得给予DHA的乙醇暴露动物与对照处理的动物不再有显著差异。因此,给予DHA可能具有治疗价值,以逆转乙醇的一些破坏作用。