Extracellular Vesicles as Promising Markers of Addictive Disorders

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Abstract

The studying the role and condition of small extracellular vesicles (sEV) in mental and addictive disorders is an extremely promising area. SEV contain proteins on the membrane that protect against destruction by their own immunity, and due to their size, they are able to cross the blood-brain barrier. These properties make it possible to consider sEV as potential biomarkers reflecting the processes occurring in the brain, and at the same time available for study in peripheral blood samples. Studies have shown that the amount, biogenesis and contents of explosives change significantly when exposed to psychoactive substances both in vitro and in vivo. The results of the analysis of modern literature demonstrate the presence of numerous potential markers of addictive pathology among the loads carried by sEV, nevertheless, the real diagnostic significance of each of them requires to be studied. Many data indicate the effect of psychoactive substances on GTPases of the Rab family, Toll-like receptors, the complement system and cytokines. Also, in several studies, sex differences in sEV changes were found in response to substance exposure. Most studies indicate the involvement of sEV in the regulation of neuroinflammatory processes, interaction between glial cells and neurons, as well as between peripheral cells and cells of the central nervous system. The authors of the review formulated a hypothesis about the presence of two mechanisms-stages in which sEV is involved: “fast” – in response to the effects of substances, providing neuroplasticity, and “slow” – the result of impaired biogenesis of sEV and the appearance of aberrant vesicle variants.

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About the authors

V. V. Severtsev

Sechenov First Moscow State Medical University; Lopukhin Federal Research and Clinical Center of Physical-Chemical Medicine of the Federal Medical Biological Agency

Author for correspondence.
Email: severtsevmed@gmail.com
Russian Federation, 119048, Moscow; 143007, Moscow

M. A. Pavkina

Sechenov First Moscow State Medical University

Email: severtsevmed@gmail.com
Russian Federation, 119048, Moscow

N. N. Ivanets

Sechenov First Moscow State Medical University

Email: severtsevmed@gmail.com
Russian Federation, 119048, Moscow

M. A. Vinnikova

Sechenov First Moscow State Medical University; Moscow Scientific and Practical Center of Narcology of the Moscow Healthcare Department

Email: severtsevmed@gmail.com
Russian Federation, 119048, Moscow; 109390, Moscow

A. A. Yakovlev

Institute of Higher Nervous Activity and Neurophysiology of the Russian Academy of Sciences; Research and Clinical Center for Neuropsychiatry of the Moscow Healthcare Department

Email: severtsevmed@gmail.com
Russian Federation, 117485, Moscow; 115419, Moscow

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2. Fig. 1. Primary endosome matures to become first a secondary endosome and then a multivesicular body. Intralumenal vesicles become exosomes after MBT fusion of Rab27 with the plasma membrane. The second pathway is the fusion of MBT with Rab7 with lysosomes and degradation of the contents

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3. Fig. 2. Place of mVB signalling in the pathogenesis of surfactant-induced changes. BDNF - brain-derived neurotrophic factor; LTD - long-term depression; LTP - long-term potentiation; AMPA - α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; NMDA - N-methyl-D-aspartate; SAW - psychoactive substance; Dyn - dynorphins; CRH - corticotropin-releasing hormone; DA - dopamine

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4. Fig. 3. Illustration of the hypothesis proposed by the authors of the review on the involvement of mVB in the pathogenesis of drug addiction diseases. The figure conventionally indicates a system of astrocyte (left), microglia (top) and neuron (right). Below the dividing line, ‘rapid changes’ are represented: 1) during the first exposures of the neuron to surfactant, synaptogenesis mechanisms are realised, triggering the release of mVBs containing factors that reduce pro-inflammatory activity and ‘requests’ for synaptogenesis support in the astrocyte; 2) the astrocyte, in response to the neuron's ‘request’, releases mVBs containing anti-inflammatory factors and factors supporting synaptogenesis; 3) this ensures consolidation of neuronal connections and a reduction in microglial cell activity; 4) in parallel, surfactants disrupt cell metabolism, leading to the accumulation of calcium and reactive oxygen species within the cell. Above the dividing line, the ‘slow changes’ are represented by: 1) the accumulation of energy and ionic disturbances leads to impaired vesicle biogenesis; 2) this results in increased production of pro-inflammatory factors and pathological proteins; 3) this in turn leads to microglia activation, reduced synaptogenesis and disruption of normal neurophysiology. ΔFosB - delta-FosB-protein; BDNF - brain-derived neurotrophic factor; Ca2+ - ionised calcium; cAMP - cyclic adenosine monophosphate; GluR - glutamate receptor; NMDAR - N-methyl-D-aspartate receptor; mt-HK - mitochondrial hexokinase; AFC - reactive oxygen species

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