Modulating effect of cytokines on mechanisms of synaptic plasticity in the brain

After accumulation of data showing that resident brain cells (neurons, astrocytes, and microglia) produce mediators of the immune system, such as cytokines and their receptors under normal physiological conditions, a critical need emerged for investigating the role of these mediators in cognitive pr...

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Vydáno v:Biochemistry (Moscow) Ročník 82; číslo 3; s. 264 - 274
Hlavní autoři: Levin, S. G., Godukhin, O. V.
Médium: Journal Article
Jazyk:angličtina
Vydáno: Moscow Pleiades Publishing 01.03.2017
Springer
Springer Nature B.V
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ISSN:0006-2979, 1608-3040, 1608-3040
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Shrnutí:After accumulation of data showing that resident brain cells (neurons, astrocytes, and microglia) produce mediators of the immune system, such as cytokines and their receptors under normal physiological conditions, a critical need emerged for investigating the role of these mediators in cognitive processes. The major problem for understanding the functional role of cytokines in the mechanisms of synaptic plasticity, de novo neurogenesis, and learning and memory is the small number of investigated cytokines. Existing concepts are based on data from just three proinflammatory cytokines: interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha. The amount of information in the literature on the functional role of antiinflammatory cytokines in the mechanisms of synaptic plasticity and cognitive functions of mature mammalian brain is dismally low. However, they are of principle importance for understanding the mechanisms of local information processing in the brain, since they modulate the activity of individual cells and local neural networks, being able to reconstruct the processes of synaptic plasticity and intercellular communication, in general, depending on the local ratio of the levels of different cytokines in certain areas of the brain. Understanding the functional role of cytokines in cellular mechanisms of information processing and storage in the brain would allow developing preventive and therapeutic means for the treatment of neuropathologies related to impairment of these mechanisms.
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ISSN:0006-2979
1608-3040
1608-3040
DOI:10.1134/S000629791703004X