Microglia and infiltrating macrophages in ictogenesis and epileptogenesis

IF 3.5 3区医学 Q2 NEUROSCIENCES

Frontiers in Molecular Neuroscience Pub Date : 2024-05-30 DOI:10.3389/fnmol.2024.1404022

Sonja Bröer, Alberto Pauletti

引用次数: 0

Abstract

Phagocytes maintain homeostasis in a healthy brain. Upon injury, they are essential for repairing damaged tissue, recruiting other immune cells, and releasing cytokines as the first line of defense. However, there seems to be a delicate balance between the beneficial and detrimental effects of their activation in a seizing brain. Blocking the infiltration of peripheral phagocytes (macrophages) or their depletion can partially alleviate epileptic seizures and prevent the death of neurons in experimental models of epilepsy. However, the depletion of resident phagocytes in the brain (microglia) can aggravate disease outcomes. This review describes the role of resident microglia and peripheral infiltrating monocytes in animal models of acutely triggered seizures and epilepsy. Understanding the roles of phagocytes in ictogenesis and the time course of their activation and involvement in epileptogenesis and disease progression can offer us new biomarkers to identify patients at risk of developing epilepsy after a brain insult, as well as provide novel therapeutic targets for treating epilepsy.

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小胶质细胞和浸润巨噬细胞在痫性发作和癫痫发生中的作用

吞噬细胞能维持健康大脑的平衡。受伤时，它们对修复受损组织、招募其他免疫细胞和释放细胞因子作为第一道防线至关重要。然而，在抽搐的大脑中，它们的激活所产生的有益和有害影响之间似乎存在着微妙的平衡。在癫痫实验模型中，阻止外周吞噬细胞（巨噬细胞）的浸润或将其耗竭可部分缓解癫痫发作并防止神经元死亡。然而，消耗大脑中的常驻吞噬细胞（小胶质细胞）会加重疾病的后果。本综述介绍了常驻小胶质细胞和外周浸润单核细胞在急性诱发癫痫发作和癫痫的动物模型中的作用。了解吞噬细胞在癫痫发生过程中的作用及其激活和参与癫痫发生和疾病进展的时间过程，可为我们提供新的生物标志物，用于识别脑损伤后有患癫痫风险的患者，并为治疗癫痫提供新的治疗靶点。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Frontiers in Molecular Neuroscience NEUROSCIENCES-

CiteScore

5.70

自引率

2.10%

发文量

669

审稿时长

14 weeks

期刊介绍： Frontiers in Molecular Neuroscience is a first-tier electronic journal devoted to identifying key molecules, as well as their functions and interactions, that underlie the structure, design and function of the brain across all levels. The scope of our journal encompasses synaptic and cellular proteins, coding and non-coding RNA, and molecular mechanisms regulating cellular and dendritic RNA translation. In recent years, a plethora of new cellular and synaptic players have been identified from reduced systems, such as neuronal cultures, but the relevance of these molecules in terms of cellular and synaptic function and plasticity in the living brain and its circuits has not been validated. The effects of spine growth and density observed using gene products identified from in vitro work are frequently not reproduced in vivo. Our journal is particularly interested in studies on genetically engineered model organisms (C. elegans, Drosophila, mouse), in which alterations in key molecules underlying cellular and synaptic function and plasticity produce defined anatomical, physiological and behavioral changes. In the mouse, genetic alterations limited to particular neural circuits (olfactory bulb, motor cortex, cortical layers, hippocampal subfields, cerebellum), preferably regulated in time and on demand, are of special interest, as they sidestep potential compensatory developmental effects.