Fetal alcohol spectrum disorder patients suffer from many cognitive disabilities. These include impaired auditory, visual, and tactile sensory information processing, making it more difficult for these patients to learn to navigate social scenarios. Rodent studies have shown that alcohol exposure during the brain growth spurt (BGS) can lead to acute neuronal apoptosis and an immunological response by microglia in the somatosensory cortex. Since microglia have critical physiological functions, including the support of excitatory synapse remodeling via interactions with dendritic spines, we sought to understand whether BGS alcohol exposure has long-term effects on microglial or dendritic spine dynamics. Using in vivo two-photon microscopy in 4–5 week old mice, we evaluated microglial functions such as process motility, the response to tissue injury, and the dynamics of physical interactions between microglial processes and dendritic spines. We also investigated potential differences in the morphology, density, or dynamics of dendritic spines in layer I/II primary sensory cortex of control and BGS alcohol exposed mice. We found that microglial process motility and contact with dendritic spines were not altered after BGS alcohol exposure. While the response of microglial processes toward tissue injury was not significantly altered by prior alcohol exposure, there was a trend suggesting that alcohol early in life may prime microglia to respond more quickly to secondary injury. Spine density, morphology, stability, and remodeling over time were not perturbed after BGS alcohol exposure. We demonstrate that after BGS alcohol exposure, the physiological functions of microglia and excitatory neurons remain intact in early adolescence.

中文翻译：

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发育性酒精暴露后早期青少年皮层小胶质细胞和树突棘的动力学

胎儿酒精谱系障碍患者患有许多认知障碍。这些包括受损的听觉、视觉和触觉感觉信息处理，使这些患者更难学会驾驭社交场景。啮齿动物研究表明，大脑生长突增 (BGS) 期间的酒精暴露可导致急性神经元凋亡和体感皮层中小胶质细胞的免疫反应。由于小胶质细胞具有关键的生理功能，包括通过与树突棘相互作用来支持兴奋性突触重塑，我们试图了解 BGS 酒精暴露是否对小胶质细胞或树突棘动力学有长期影响。在 4-5 周龄小鼠体内使用双光子显微镜，我们评估了小胶质细胞的功能，如过程运动、对组织损伤的反应、以及小胶质细胞过程和树突棘之间物理相互作用的动力学。我们还研究了对照组和 BGS 酒精暴露小鼠 I/II 层初级感觉皮层中树突棘的形态、密度或动力学的潜在差异。我们发现，在 BGS 酒精暴露后，小胶质细胞的运动性和与树突棘的接触没有改变。虽然小胶质细胞过程对组织损伤的反应并没有因之前的酒精暴露而显着改变，但有一种趋势表明，生命早期的酒精可能会促使小胶质细胞对继发性损伤做出更快的反应。在 BGS 酒精暴露后，脊柱密度、形态、稳定性和随时间的重塑没有受到干扰。我们证明，在 BGS 酒精暴露后，