MODULATING EFFECT OF CYTOKINES ON MECHANISMS OF SYNAPTIC PLASTICITY IN THE BRAIN
Recent studies have shown that neurons and glia cells from the brain are also capable of producing cytokines and their receptors, and these cytokines mediate essential brain functions during health that lie outside their functions in traditional immune and inflammatory processes. At present, however, it has become clear that many immune molecules (cytokines) can be used constitutively by the brain as signaling molecules involved in molecular and cellular mechanisms serving synaptic plasticity and memory formation. However, the major limitation of the research on this topic is the relatively few cytokines for which sufficient evidence of their effects related to synaptic plasticity as well as learning and memory processes. Most of the research has focused on the involvement of proinflammatory cytokines, such as interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha. In particular, we have no data about the role of antiinflammatory cytokines in the mechanisms of modulation of synaptic plasticity and cognitive functions in the adult mammalian brain. The main goal of this review article is to investigate the mechanisms of modulation of two forms of synaptic plasticity, LTP and homeostatic plasticity, by pro- and antiinflammatory cytokines. Furthermore, study of canonical and noncanonical signaling cascades through which cytokines mediate synaptic modulation are analyzed. The results of this work elucidate conceptual and mechanistic issues pertaining to the role of different cytokines in neuronal and neurobehavioral plasticity.