The current study further examined the effect of the muscarinic acetylcholine antagonist, scopolamine, on the Context Preexposure Facilitation Effect (CPFE; Robinson-Drummer, Dokovna, Heroux, & Stanton, 2016). In the CPFE, context representations formed during the preexposure phase are retrieved and associated with immediate shock during the training phase and expressed as freezing during a 24-hr retention phase. Scopolamine abolished postshock and retention freezing when administered systemically prior to preexposure (Experiment 1A) or immediate-shock training (Experiment 1B). Pretraining infusion of scopolamine into dorsal hippocampus (dHPC) disrupted both postshock and retention freezing (Experiments 2A) and retention freezing when the postshock freezing test was omitted (Experiment 2B) but did not alter expression of freezing behavior to an auditory fear stimulus (Experiment 2C). Finally, pretraining scopolamine infusion into ventral hippocampus (vHPC) also abolished postshock and retention test freezing (Experiment 3). These findings suggest similar roles for muscarinic receptor activity in both the dHPC and vHPC in the CPFE. This study advances understanding of the neurobiology of the CPFE by showing that context-shock associations are not learned following disruption of the cholinergic and/or hippocampal function on either the preexposure or training day. Existing theories of the CPFE (Rudy, 2009) have inferred this effect based on impaired 24-hr retention observed in previous studies (Matus-Amat, Higgins, Barrientos, & Rudy, 2004; Robinson-Drummer et al., 2016). However, the present study is the first to demonstrate it directly by including a postshock freezing measure. Further, this study is the first to identify vHPC as another important region necessary for context-shock learning during the CPFE paradigm. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

中文翻译：

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背侧和腹侧海马毒蕈碱受体活性在情境恐惧条件反射的获得和保留中的作用。

目前的研究进一步检查了毒蕈碱乙酰胆碱拮抗剂东莨菪碱对环境暴露前促进效应的影响 (CPFE; Robinson-Drummer, Dokovna, Heroux, & Stanton, 2016)。在 CPFE 中，在暴露前阶段形成的上下文表示被检索并与训练阶段的即时电击相关联，并在 24 小时保留阶段表示为冻结。在暴露前（实验 1A）或即刻休克训练（实验 1B）之前全身给药时，东莨菪碱消除了休克后和滞留冻结。训练前将东莨菪碱输注到背侧海马体 (dHPC) 会破坏休克后和保留冷冻（实验 2A）以及在省略休克后冷冻测试时保留冷冻（实验 2B），但没有改变冷冻行为对听觉恐惧刺激的表达（实验 2C） ）。最后，训练前将东莨菪碱输注到腹侧海马体 (vHPC) 也消除了休克后和保留试验冻结（实验 3）。这些发现表明毒蕈碱受体活性在 CPFE 中的 dHPC 和 vHPC 中具有相似的作用。这项研究表明，在暴露前或训练日胆碱能和/或海马功能受到破坏后，不会学习上下文休克关联，从而促进了对 CPFE 神经生物学的理解。CPFE 的现有理论 (Rudy, 2009 年）根据先前研究中观察到的 24 小时保留受损推断出这种影响（Matus-Amat、Higgins、Barrientos 和 Rudy，2004 年；Robinson-Drummer 等人，2016 年）。然而，本研究首次通过包括震后冻结措施直接证明了这一点。此外，这项研究首次将 vHPC 确定为 CPFE 范式期间上下文冲击学习所需的另一个重要区域。（PsycInfo 数据库记录 (c) 2020 APA，保留所有权利）。这项研究首次将 vHPC 确定为 CPFE 范式期间上下文冲击学习所需的另一个重要区域。（PsycInfo 数据库记录 (c) 2020 APA，保留所有权利）。这项研究首次将 vHPC 确定为 CPFE 范式期间上下文冲击学习所需的另一个重要区域。（PsycInfo 数据库记录 (c) 2020 APA，保留所有权利）。