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Neuronal integrity, not activity, drives synaptic material clearance by microglia after CNS injury

ABSTRACT: Neuronal integrity, not activity, drives synaptic material clearance by microglia after CNS injury

PROVIDER: PRJNA420938 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6340190_1.fastq.gz	Fastqsanger.gz
	SRR6340190_2.fastq.gz	Fastqsanger.gz
	SRR6340200_1.fastq.gz	Fastqsanger.gz
	SRR6340200_2.fastq.gz	Fastqsanger.gz
	SRR6340191_1.fastq.gz	Fastqsanger.gz

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Neuronal integrity, not activity, drives synaptic material clearance by microglia after CNS injury

Project description:Phagocytosis of synaptic debris by microglia is critical for CNS development and homeostasis. Less well understood are microglial functions in injured adult brain, where their presumed role is clearance of neuronal debris. Assay of this process is challenging, because the resulting peripheral myeloid-cell engraftment is difficult to dissociate from microglial clearance. The model used here, optic nerve crush injury in adult mouse, stimulates rapid engulfment of synaptic material by microglia residing in the lateral geniculate nucleus (LGN), sufficiently distant from the injury to preclude peripheral-cell engraftment. Pre-injury pharmacological depletion of microglia causes post-injury accumulation of synaptic debris, suggesting that these, not astrocytes, are the dominant post-injury phagocytes. Genetic and pharmacological manipulations revealed that neuronal activity, which regulates microglial engulfment of synaptic debris in development, does not do so in post-injury synaptic material clearance in adulthood, where such clearance depends instead on axonal integrity. RNAseq reveals C1q involvement in clearance of debris by LGN-resident microglia, supporting our finding of its impaired clearance in C1qa-/- and Itgam-/- mice. Our results demonstrate how neurodegenerative debris is cleared by microglial phagocytosis, and offer a model for assaying microglial phagocytic activity and studying its mechanisms and physiological roles.

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Project description:Phagocytosis of synaptic material by microglia is critical for central nervous system development. Less well understood is this microglial function in the injured adult brain. Assay of microglial phagocytosis is challenging, because peripheral myeloid cells engraft the site of injury, which could obscure interpretation of microglial roles. The model used here, optic nerve crush injury, results in degeneration of synapses in the dorsal lateral geniculate nucleus (dLGN), which stimulates rapid activation and engulfment of synaptic material by resident microglia without myeloid cell engraftment. Pharmacological depletion of microglia causes postinjury accumulation of synaptic debris, suggesting that microglia are the dominant postinjury phagocytes. Genetic or pharmacological manipulations revealed that neuronal activity does not trigger microglia phagocytosis after injury. RNA sequencing reveals C1q and CD11b/CR3 involvement in clearance of debris by dLGN-resident microglia. Indeed, C1qa-/- and Itgam-/- mice exhibit impaired postinjury debris clearance. Our results show how neurodegenerative debris is cleared by microglia and offers a model for studying its mechanisms and physiological roles.

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