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Outward depolarization of the microglia mitochondrial membrane potential following lipopolysaccharide exposure: a novel screening tool for microglia metabolomics. | LitMetric

Outward depolarization of the microglia mitochondrial membrane potential following lipopolysaccharide exposure: a novel screening tool for microglia metabolomics.

Front Cell Neurosci

Department of Psychology, Psychological and Brain Sciences & Interdisciplinary Neuroscience Programs, College of Liberal Arts, University of Nevada, Las Vegas, NV, United States.

Published: November 2024

AI Article Synopsis

Article Abstract

Microglia are non-electrogenic immune cells that respond rapidly to protect the central nervous system (CNS) from infections, injuries, or other forms of damage. Microglia mitochondria are essential for providing the requisite energy resources for immune regulation. While fluctuations in energy metabolism are regulated by mitochondria and are reflected in the mitochondrial membrane potential (ΔΨm), there remains a lack of innovation in microglia-centric tools that capitalize on this. In this study, live imaging of microglia in acute slices from EGFP reporter mice expressing EGFP under the control of the fractalkine receptor (CX3CR1) promoter is combined with loading a fluorescent reporter of ΔΨm. Depolarizations in the ΔΨm were recorded after administering the well-characterized immune stimulant lipopolysaccharide (LPS). Microglia ΔΨm increased in distinctive phases with a relatively steep slope following LPS exposure. Conversely, the ΔΨm of neurons showed minimal regulation, highlighting a distinct microglia ΔΨm response to immune stimuli. Analysis of the depolarization of the microglia ΔΨm in the soma, branches, and endfeet revealed progressive changes in each subcellular domain originating in the soma and progressing outward. The inverse agonist emapunil attenuated the depolarization of the ΔΨm across states in a domain-specific manner. These findings emphasize the contribution of mitochondrial membrane dynamics in regulating microglial responses to immune stimuli. Further, this work advances a novel drug screening strategy for the therapeutic regulation of metabolic activity in inflammatory conditions of the brain.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11576292PMC
http://dx.doi.org/10.3389/fncel.2024.1430448DOI Listing

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