Fig. 2

Roles of extracellular vesicles (EVs) in the central nervous system (CNS) after insult. Almost all CNS cells can secrete and uptake EVs containing various bioactive molecules, which affect receptor cell function under various physiological and pathological conditions. Neurons can release EVs to other neurons, thereby modulating synaptic plasticity in the CNS. Activated microglia/EV complexes containing miR-146a-5p can be internalized by neurons, in which they reduce the synaptic density under inflammatory conditions. Moreover, neuronal EVs can upregulate the expression of complement component 3 in microglia, thereby enhancing its phagocytic and synaptic pruning abilities under both developmental and pathological conditions. Neuronal EVs containing miR-124a act on astrocytes to regulate extracellular glutamate concentrations. Activated astrocytes release EVs carrying synaptophysin, which acts on neurons to promote neuronal growth under conditions of high neuronal activity and/or oxidative stress. Furthermore, neuronal exosomal miR-132 interacts with endothelial cells, which maintained the integrity of the blood–brain barrier in an intact zebrafish larvae model. Polarization of neurons can prompt oligodendrocytes to release more EVs, which enhanced neuronal tolerance and firing frequency in a model of cerebral ischemia. EVs also act on oligodendrocytes, thereby inhibiting their differentiation and myelination. In addition, glial cells in the CNS and immune cells in the peripheral nervous system can modulate the inflammatory response after nerve injury through extensive communication mediated by EVs