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

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.V modeli vyrabotki ustoĭchivosti neĭronov k toksicheskomu deĭstviiu glutamata (predvaritel'naia deprivatsiia troficheskikh faktorov) prodemonstrirovana sekretsiia ékzosom. Sekretsiia ékzosom proiskhodit na étape vyrabotki ustoĭchivosti pri prekonditsionirovanii i pri posleduiushcheĭ stadii zakrepleniia vyrabotannoĭ ustoĭchivosti v techenie sutok posle prekonditsionirovaniia, éto bylo pokazano s ispol'zovaniem immunokhimicheskogo okrashivaniia vnekletochnoĭ zhidkosti na marker ékzosom belok CD63. Ingibitor autofagii bafilomitsin v kontsentratsii 0,01 mkM dostoverno snizhaet vyrazhennost' sekretsii ékzosom kak na étape vyrabotki autofagii, tak i v techenie pervykh sutok posle vyrabotki. Pri étom ingibirovanie autofagii vo vremia deprivatsii troficheskikh faktorov predotvrashchaet vyrabotku ustoĭchivosti, a ingibirovanie autofagii v techenie pervykh sutok posle deprivatsii ne vliiaet na vyrabotku ustoĭchivosti. My predpolagaem, chto dolgovremennye éffekty prekonditsionirovaniia mogut byt' oposredovany sekretsieĭ ékzosom.