Phagolysosomal activity of microglia in the sleep deprived mouse hippocampus




Burns, Sophia

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Much of the population gets an insufficient amount of sleep. However, sleep deprivation (SD) can lead to detrimental consequences including the impairment of hippocampal processes such as memory and cognition. Recent studies revealed synaptic deficits in the Cornu Ammonis (CA)1 region of the hippocampus, but not the CA3 region, following acute SD. Microglia, the resident immune cells of the brain, are important players for synaptic plasticity and are known to be affected by SD. This study aims to determine the microglial mechanism involved in the hippocampal region-dependent synaptic deficits following acute SD, focusing on their phagolysosomal activity. To do so, C57BL/6J male mice were sleep-deprived for 5 hours by gentle handling. Using immunofluorescence against IBA1, a microglia/macrophages marker, and TMEM119, a microglia-specific marker, we were able to determine that acute SD does not cause region-dependent macrophage infiltration. We then investigated the phagolysosomal pathway using double immunofluorescence against IBA1 and CD68, a phagolysosomal marker, and confocal microscopy. Finally, we investigated microglial ultrastructural changes using scanning electron microscopy. A deeper understanding of the mechanisms behind cognitive deficits following acute SD opens the possibility for the development of therapeutic strategies that can improve the lives of individuals who suffer the consequences of sleep loss.



Microglia, phagolysosomal activity, neuroplasticity, sleep deprivation, neuroscience, electron microscopy, confocal imaging, brightfield imaging, immunofluorescence, immune cells, mouse hippocampus