AIMS Recent studies have recognized that thalamic nucleus reuniens (Re) undergoes substantial neuron loss following alcohol exposure (AE) during the brain growth spurt (BGS). As all previous studies have utilized high-dose AE paradigms, we tested whether moderate-dose AE is capable of damaging Re to a similar degree as high-dose AE. METHODS We used a rat model of third-trimester binge AE (relative to human pregnancy) to administer ethanol to rat pups at either a high (5.25 g/kg/day) or moderate (3.00 g/kg/day) dose during the BGS (postnatal days [PD] 4-9) via intragastric intubation. In adulthood (i.e. PD72), we quantified the volume of Re as well as the total number of neurons and non-neuronal cells in the nucleus (which were further divided into microglia versus 'other' non-neurons), using unbiased stereological estimation of cells identified with immunofluorescent markers (i.e. nuclear label Hoechst, neuron-specific protein NeuN, and microglia-specific protein Iba1). Data were analyzed both between-treatment and correlated with peak blood alcohol concentration (BAC). RESULTS AND CONCLUSIONS We observed significant neuronal and non-neuronal cell loss in both the high-dose and moderate-dose AE groups (relative to both procedural control and typically-developing control groups), which mediated reductions in Re volume. Outcomes did not correlate with peak BAC, further supporting that Re is vulnerable to AE-induced neurodegeneration at lower doses than previously suspected. Given the role that Re has in coordinating prefrontal cortex and hippocampus, the current study highlights the role that thalamic damage may play in the range of behavioral alterations observed in Fetal Alcohol Spectrum Disorders.

中文翻译：

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妊娠晚期酒精暴露的大鼠模型在中等剂量与高剂量侮辱后会在丘脑 Reuniens 中产生类似的终生变化。

目的 最近的研究已经认识到，在大脑生长突增 (BGS) 期间接触酒精 (AE) 后，丘脑核团聚核 (Re) 会经历大量神经元损失。由于所有以前的研究都使用高剂量 AE 范例，我们测试了中等剂量 AE 是否能够将 Re 破坏到与高剂量 AE 相似的程度。方（产后天 [PD] 4-9）通过胃内插管。在成年期（即 PD72），我们量化了 Re 的体积以及细胞核中神经元和非神经元细胞的总数（进一步分为小胶质细胞与“其他”非神经元），使用免疫荧光标记物（即核标记 Hoechst、神经元特异性蛋白 NeuN 和小胶质细胞特异性蛋白 Iba1）鉴定的细胞的无偏体视学估计。数据在治疗之间进行了分析，并与峰值血液酒精浓度 (BAC) 相关联。结果和结论 我们在高剂量和中等剂量 AE 组（相对于程序控制组和典型发育对照组）均观察到显着的神经元和非神经元细胞丢失，这介导了 Re 体积的减少。结果与峰值 BAC 无关，进一步支持 Re 易受 AE 诱导的神经变性的影响，剂量低于先前怀疑的剂量。鉴于 Re 在协调前额叶皮层和海马体中的作用，