The morphology of microglial cells is often closely related to their functions. The mechanisms that regulate microglial ramification are not well understood. Here we reveal the biological mechanisms by which astrocytes regulate microglial ramification. Morphological variation in mouse microglial cultures was measured in terms of cell area as well as branch number and length. Effects on microglial ramification were analyzed after microinjecting the toxin L-alpha-aminoadipic acid (L-AAA) in the mouse cortex or hippocampus to ablate astrocytes, and after culturing microglia on their own in an astrocyte-conditioned medium (ACM) or together with astrocytes in coculture. TGF-β expression was determined by Western blotting, immunohistochemistry, and ELISA. The TGF-β signaling pathway was blocked by the TGF-β antibody to assess the role of TGF-β on microglial ramification. The results showed that microglia had more and longer branches and smaller cell bodies in brain areas where astrocytes were abundant. In the mouse cortex and hippocampus, ablation of astrocytes by L-AAA decreased number and length of microglial branches and increased the size of cell bodies. Similar results were obtained with isolated microglia in culture. However, isolated microglia were able to maintain their multibranched structure for a long time when cultured on astrocyte monolayers. Ameboid microglia isolated from P0 to P3 mice showed increased ramification when cultured in ACM or on astrocyte monolayers. Microglia cultured on astrocyte monolayers showed more complex branching structures than those cultured in ACM. Blocking astrocyte-derived TGF-β decreased microglial ramification. Astrocytes induced the formation of protuberances on branches of microglia by forming glial fibers that increased traction. These experiments in mice suggest that astrocytes promote microglial ramification by forming glial fibers to create traction and by secreting soluble factors into the surroundings. For example, astrocyte-secreted TGF-β promotes microglia to generate primitive branches, whose ramification is refined by glial fibers.
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http://dx.doi.org/10.3389/fncel.2020.00195 | DOI Listing |
eNeuro
January 2025
University of Rochester Medical Center, Department of Neuroscience,
A unique pool of immature glutamatergic neurons in the primate amygdala, known as the paralaminar nucleus (PL), are maturing between infancy and adolescence. The PL is a potential substrate for the steep growth curve of amygdala volume during this developmental period. A microglial component is also embedded among the PL neurons, and likely supports local neuronal maturation and emerging synaptogenesis.
View Article and Find Full Text PDFLab Chip
December 2024
Laboratory of Cell Biology and Histology, Faculty of Biomedical, Pharmaceutical and Veterinary sciences, University of Antwerp, Universiteitsplein 1, Antwerp, Belgium.
Modern cell and developmental biology increasingly relies on 3D cell culture systems such as organoids. However, routine interrogation with microscopy is often hindered by tedious, non-standardized sample mounting, limiting throughput. To address these bottlenecks, we have developed a pipeline for imaging intact organoids in flow, utilizing a transparent agarose fluidic chip that enables efficient and consistent recordings with theoretically unlimited throughput.
View Article and Find Full Text PDFBrain Circ
September 2024
Department of Neurology, Minnesota Medical School, Minneapolis, MN, USA.
Background: Alzheimer's Disease is a neurodegenerative disease characterized by accumulation of phosphorylated tau and amyloid deposits within the brain tissues in the elderly population. Numerous studies established that amassment of these toxic accretions within the brain tissues initiates neuronal demise and synaptic impairment which becomes the underlying basis for memory loss and cognitive abnormalities in these patients.
Hypothesis: Hypoxia, oxidative stress, and inflammation are commonly encountered perils in the neuronal milieu that derail the neuron-synapse interactions and maneuver them to undergo apoptosis.
Glia
December 2024
SLEEPWELL Research Program I Faculty of Medicine, University of Helsinki, Finland.
Microglia, the resident immune cells in the brain, dynamically adapt their morphology based on their functional state. This study explored the relationship between microglial morphology and sleep-wake cycles in mice. Using Iba1 immunostaining to identify microglia, we quantified morphological changes in microglia at different timepoints in multiple brain regions (cortex, hippocampus, basal forebrain, hindbrain, and cerebellum) in B6 male mice using semi-automated 3D structural analysis.
View Article and Find Full Text PDFPolymers (Basel)
August 2024
Department of Chemical and Pharmaceutical Engineering, College of Chemical Engineering, Huaqiao University, Xiamen 361021, China.
Microglia respond to stressors by secreting cytokines or growth factors, playing a crucial role in maintaining brain homeostasis. While the antidepressant-like effects of polysaccharides (PSPs) have been observed in mice, their potential effectiveness involving microglial regulation remains unknown. This study investigates the antidepressant-like mechanism of PSP by regulating microglial phenotype and signaling pathways in the prefrontal cortex of chronic restraint stress (CRS)-induced mice.
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