Long-term Reductions in the Population of GABAergic Interneurons in the Mouse Hippocampus following Developmental Ethanol Exposure.
Long-term Reductions in the Population of GABAergic Interneurons in the Mouse Hippocampus following Developmental Ethanol Exposure.
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DOI：
10.1016/j.neuroscience.2018.05.003
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发表时间：
2018-07-15
期刊：
影响因子：
3.3
通讯作者：
Valenzuela CF
中科院分区：
文献类型：
--
作者：
Bird CW;Taylor DH;Pinkowski NJ;Chavez GJ;Valenzuela CF
发育过程中接触乙醇会导致一系列认知和行为异常，称为胎儿酒精谱系障碍(FASD)。孕期酒精暴露对中枢神经系统的许多细胞类型都有负面影响，包括抑制性GABA能中间神经元。然而，几乎没有证据描述胎儿酒精暴露对海马结构内中间神经元存活的长期影响，这对FASD患者的学习和记忆过程是至关重要的。在相当于人类妊娠的晚期(出生后2-9天)，将在抑制性中间神经元中表达金星黄色荧光蛋白的小鼠暴露于汽化乙醇中，并在第90天用无偏倚体视学方法测量对中间神经元数量的长期影响。成年后，每个被检查的海马区的中间神经元数量都减少了。此外，我们还发现，一次暴露于P7的乙醇引起了海马门区、颗粒细胞层、CA1区和CA3区中间神经元凋亡性神经元变性的强烈激活。这些研究表明，发育性酒精暴露对海马神经元间存活能力有长期影响，并可能提供一种机制，部分解释FASD患者的海马区功能缺陷和海马区依赖行为。
Developmental exposure to ethanol leads to a constellation of cognitive and behavioral abnormalities known as Fetal Alcohol Spectrum Disorders (FASDs). Many cell types throughout the central nervous system are negatively impacted by gestational alcohol exposure, including inhibitory, GABAergic interneurons. Little evidence exists, however, describing the long-term impact of fetal alcohol exposure on survival of interneurons within the hippocampal formation, which is critical for learning and memory processes that are impaired in individuals with FASDs. Mice expressing Venus yellow fluorescent protein in inhibitory interneurons were exposed to vaporized ethanol during the third trimester equivalent of human gestation (postnatal days 2-9), and the long-term effects on interneuron numbers were measured using unbiased stereology at P90. In adulthood, interneuron populations were reduced in every hippocampal region examined. Moreover, we found that a single exposure to ethanol at P7 caused robust activation of apoptotic neurodegeneration of interneurons in the hilus, granule cell layer, CA1 and CA3 regions of the hippocampus. These studies demonstrate that developmental ethanol exposure has a long-term impact on hippocampal interneuron survivability, and may provide a mechanism partially explaining deficits in hippocampal function and hippocampal dependent behaviors in those afflicted with FASDs.
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影响因子：
2.9
作者：
Hamilton GF;Murawski NJ;St Cyr SA;Jablonski SA;Schiffino FL;Stanton ME;Klintsova AY
通讯作者：
Klintsova AY
影响因子：
7.2
作者：
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通讯作者：
Ravichandran, Kodi S.
影响因子：
2
作者：
Gundersen, HJG;Jensen, EBV;Nielsen, J
通讯作者：
Nielsen, J
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5.3
作者：
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通讯作者：
Sheng, Morgan
影响因子：
64.8
作者：
COBB, SR;BUHL, EH;SOMOGYI, P
通讯作者：
SOMOGYI, P