Microglial cells (resident macrophages) feature rapid activation in CNS disease and can acquire multiple phenotypes exerting neuroprotection or neurotoxicity. The functional impact of surveying (“resting”) microglia on neural excitability and neurotransmission in physiology is widely unknown, however. We addressed this issue in male rat hippocampal slice cultures (in situ) by pharmacological microglial ablation within days and by characterizing neuronal gamma‐band oscillations (30–70 Hz) that are highly sensitive to neuromodulators and disturbances in ion and energy regulation. Gamma oscillations support action potential timing and synaptic plasticity, associate with higher brain functions like perception and memory, and require precise communication between excitatory pyramidal cells and inhibitory (GABAergic) interneurons. The slice cultures featured well‐preserved hippocampal cytoarchitecture and parvalbumin‐positive interneuron networks, microglia with ramified morphology, and low basal levels of IL‐6, TNF‐α, and nitric oxide (NO). Stimulation of slice cultures with the pro‐inflammatory cytokine IFN‐γ or bacterial LPS serving as positive controls for microglial reactivity induced MHC‐II expression and increased cytokine and NO release. Chronic exposure of slice cultures to liposome‐encapsulated clodronate reduced the microglial cell population by about 96%, whereas neuronal structures, astrocyte GFAP expression, and basal levels of cytokines and NO were unchanged. Notably, the properties of gamma oscillations reflecting frequency, number and synchronization of synapse activity were regular after microglial depletion. Also, electrical stimulus‐induced transients of the extracellular potassium concentration ([K⁺]_o) reflecting cellular K⁺ efflux, clearance and buffering were unchanged. This suggests that nonreactive microglia are dispensable for neuronal homeostasis and neuromodulation underlying network signaling and rhythm generation in cortical tissue.

中文翻译：

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神经元伽马振荡和活动依赖性钾瞬变在出生后皮质组织中的小胶质细胞耗尽后保持规律。

小胶质细胞（常驻巨噬细胞）在 CNS 疾病中具有快速激活的特征，并且可以获得多种表型，发挥神经保护作用或神经毒性。然而，在生理学中测量（“静止”）小胶质细胞对神经兴奋性和神经传递的功能影响广为人知。我们通过几天内的药理学小胶质细胞消融和表征对神经调节剂和离子和能量调节紊乱高度敏感的神经元伽马波段振荡（30-70 Hz），在雄性大鼠海马切片培养（原位）中解决了这个问题。伽马振荡支持动作电位计时和突触可塑性，与感知和记忆等高级大脑功能相关，并且需要兴奋性锥体细胞和抑制性（GABA 能）中间神经元之间的精确通信。切片培养物具有保存完好的海马细胞结构和小清蛋白阳性中间神经元网络、具有分支形态的小胶质细胞以及低基础水平的 IL-6、TNF-α 和一氧化氮 (NO)。用促炎细胞因子 IFN-γ 或细菌 LPS 刺激切片培养物作为小胶质细胞反应性的阳性对照，诱导 MHC-II 表达并增加细胞因子和 NO 释放。切片培养物长期暴露于脂质体包裹的氯膦酸盐可使小胶质细胞数量减少约 96%，而神经元结构、星形胶质细胞 GFAP 表达以及细胞因子和 NO 的基础水平没有变化。值得注意的是，伽马振荡反映突触活动的频率、数量和同步的特性在小胶质细胞耗竭后是有规律的。还，⁺ ] _o ) 反映细胞 K ⁺流出、清除和缓冲没有变化。这表明非反应性小胶质细胞对于皮层组织中网络信号传导和节律生成的神经元稳态和神经调节是可有可无的。