Exosomes secretion and autophagy in long-term protection of neurons from excitotoxic damage

Abstract

In the model of induced neuronal resistance to the toxic effect of glutamate (deprivation of trophic factors), exosome secretion is demonstrated. Exosomes are secreted at the development of resistance during deprivation and at the first 24 h after preconditioning, as was shown by dot blot of extracellular fluid using anti-CD63 antibody. The autophagy inhibitor bafilomycin (0.01 μM) significantly reduces the quantity of the secreted exosomes at the stage of autophagy induction and at 24 h after induction. At the same time, inhibition of autophagy during the deprivation of trophic factors prevents the development of resistance, but inhibition of autophagy during the first 24 h after deprivation does not affect the development of resistance. We suggest that the long-term effects of preconditioning may be mediated by exosome secretion.

The Neuroprotection Effects of Exosome in Central Nervous System Injuries: a New Target for Therapeutic Intervention

“…The functions of exosomes in excitotoxicity have also been well established. It has been shown that longterm secretion of exosomes protected neurons from excitotoxic damage in the model of trophic factors deprivation [139]. Besides, astrocyte-derived exosomes suppressed glutamate-induced hippocampal neuron death in an in vitro glutamate excitotoxicity model [140].…”