Systemic LPS-induced microglial activation results in increased GABAergic tone: A mechanism of protection against neuroinflammation in the medial prefrontal cortex in mice.
Jinxiang Jiang,Binliang Tang,Lei Wang,Qingwei Huo,Shuyi Tan,Afzal Misrani,Yuanyuan Han,Hui-dong Li,Hai-Dong Hu,Jichen Wang,Tinghui Cheng,Sidra Tabassum,Ming Chen,Wenyuan Xie,Cheng Long,Li Yang +15 more
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TLDR
In this article, the authors report that acute neuroinflammation induced by intraperitoneal injection of lipopolysaccharide (LPS) results in cell-type-specific increases in inhibitory postsynaptic currents in the glutamatergic, but not the GABAergic, neurons of medial prefrontal cortex (mPFC), coinciding with excessive microglial activation.Abstract:
Neuroinflammation with excess microglial activation and synaptic dysfunction are early symptoms of most neurological diseases. However, how microglia-associated neuroinflammation regulates synaptic activity remains obscure. We report here that acute neuroinflammation induced by intraperitoneal injection of lipopolysaccharide (LPS) results in cell-type-specific increases in inhibitory postsynaptic currents in the glutamatergic, but not the GABAergic, neurons of medial prefrontal cortex (mPFC), coinciding with excessive microglial activation. LPS causes upregulation in levels of GABAAR subunits, glutamine synthetase and vesicular GABA transporter, and downregulation in brain-derived neurotrophic factor (BDNF) and its receptor, pTrkB. Blockage of microglial activation by minocycline ameliorates LPS-induced abnormal expression of GABA signaling-related proteins and activity of synaptic and network. Moreover, minocycline prevents the mice from LPS-induced aberrant behavior, such as a reduction in total distance and time spent in the centre in the open field test; decreases in entries into the open arm of elevated-plus maze and in consumption of sucrose; increased immobility in the tail suspension test. Furthermore, upregulation of GABA signaling by tiagabine also prevents LPS-induced microglial activation and aberrant behavior. This study illustrates a mode of bidirectional constitutive signaling between the neural and immune compartments of the brain, and suggests that the mPFC is an important area for brain-immune system communication. Moreover, the present study highlights GABAergic signaling as a key therapeutic target for mitigating neuroinflammation-induced abnormal synaptic activity in the mPFC, together with the associated behavioral abnormalities.read more
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Human neural stem cells secretome inhibits lipopolysaccharide-induced neuroinflammation through modulating microglia polarization by activating PPAR-γ.
Jiqin Zhou,Wei Ni,Yating Ling,Xiaorui Lv,Dong-Yu Niu,Yu Zeng,Yun-Tan Qiu,Yu Si,Ziyu Wang,Jiabo Hu +9 more
TL;DR: NSC-S promotes the regression of LPS-induced microglia-mediated inflammation through the PPAR-γ pathway through which the fatty acid binding protein 5 (FABP5) may mediate PPar-γ activation and inflammation remission.
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The Key Drivers of Brain Injury by Systemic Inflammatory Responses after Sepsis: Microglia and Neuroinflammation
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TL;DR: A systematic review of retrospective studies which exclusively focuses on the inflammatory mechanisms of sepsis-associated encephalopathy (SAE) has been provided in this article , which summarizes the recent advance in the field of neuroinflammation and sheds light on activation of microglia in SAE.
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Immune signaling in sex-specific neural and behavioral development: Adolescent opportunity
TL;DR: In this article , the authors review well-defined examples of sex differences during adolescence and then survey the literature to speculate how immune signaling might be playing a role in defining sex-specific adolescent outcomes.
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Minocycline Ameliorates Chronic Unpredictable Mild Stress-Induced Neuroinflammation and Abnormal mPFC-HIPP Oscillations in Mice
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Neural mechanism underlies CYLD modulation of morphology and synaptic function of medium spiny neurons in dorsolateral striatum
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