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在妊娠晚期胎儿酒精暴露的啮齿动物模型中,丘脑 reunions 核中前额叶轴突传出纤维的表现。

Representation of prefrontal axonal efferents in the thalamic nucleus reuniens in a rodent model of fetal alcohol exposure during third trimester.

作者信息

Smith Ian F, Gursky Zachary H, Klintsova Anna Y

机构信息

Department of Psychological and Brain Sciences, University of Delaware, Newark, DE, United States.

Interdisciplinary Neuroscience Graduate Program, University of Delaware, Newark, DE, United States.

出版信息

Front Behav Neurosci. 2022 Sep 8;16:993601. doi: 10.3389/fnbeh.2022.993601. eCollection 2022.

DOI:10.3389/fnbeh.2022.993601
PMID:36160686
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9493097/
Abstract

Alcohol exposure (AE) during the prenatal period could result in fetal alcohol spectrum disorders (FASDs), one of many deficits of which is impaired executive functioning (EF). EF relies on the coordination of activity between the medial prefrontal cortex (mPFC) and hippocampus (HPC) by the thalamic nucleus reuniens (Re), a structure that has been shown to be damaged following high-dose AE in a rodent model of third trimester exposure. Notably, mPFC neurons do not project directly to HPC, but rather communicate with it a disynaptic pathway where the first cortical axons synapse on neurons in Re, which in turn send axons to make contacts with hippocampal cells. This experiment investigated the effect of binge AE (5.25 g/kg/day, two doses 2 h apart) during postnatal days 4-9 on the length of medial prefrontal axonal projections within Re in Long Evans rat. AE reduced the cumulative length of mPFC-originating axon terminals in Re in female rats, with male rats exhibiting shorter cumulative lengths when compared to female procedural control animals. Additionally, Re volume was decreased in AE animals, a finding that reproduced previously reported data. This experiment helps us better understand how early life AE affects prefrontal-thalamic-hippocampal connectivity that could underlie subsequent EF deficits.

摘要

孕期酒精暴露(AE)可能导致胎儿酒精谱系障碍(FASDs),其中诸多缺陷之一是执行功能(EF)受损。EF依赖于丘脑连合核(Re)对内侧前额叶皮质(mPFC)和海马体(HPC)之间活动的协调,在孕晚期暴露的啮齿动物模型中,高剂量AE后该结构已被证明受损。值得注意的是,mPFC神经元并不直接投射到HPC,而是通过一个双突触通路与之通信,其中第一批皮质轴突在Re中的神经元上形成突触,Re中的神经元继而发出轴突与海马体细胞建立联系。本实验研究了出生后第4至9天暴饮暴食型AE(5.25克/千克/天,两剂,间隔2小时)对Long Evans大鼠中Re内内侧前额叶轴突投射长度的影响。AE减少了雌性大鼠Re中源自mPFC的轴突终末的累积长度,与雌性程序对照动物相比,雄性大鼠的累积长度更短。此外,AE动物的Re体积减小,这一发现重现了先前报道的数据。本实验有助于我们更好地理解早期生活中的AE如何影响前额叶 - 丘脑 - 海马体连接,而这种连接可能是随后EF缺陷的基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b455/9493097/9e6a2095b1df/fnbeh-16-993601-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b455/9493097/81a3f935b56c/fnbeh-16-993601-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b455/9493097/9e6a2095b1df/fnbeh-16-993601-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b455/9493097/81a3f935b56c/fnbeh-16-993601-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b455/9493097/9e6a2095b1df/fnbeh-16-993601-g002.jpg

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