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      IL-6 regulation of synaptic function in the CNS.

      1
      Neuropharmacology
      Elsevier BV
      Ca(2+), Cerebellum, Cognitive function, Glia, Hippocampus, JAK/STAT, MAPK, Memory, NMDA, Neurologic disorders

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          Abstract

          A growing body of evidence supports a role for glial-produced neuroimmune factors, including the cytokine IL-6, in CNS physiology and pathology. CNS expression of IL-6 has been documented in the normal CNS at low levels and at elevated levels in several neurodegenerative or psychiatric disease states as well as in CNS infection and injury. The altered CNS function associated with these conditions raises the possibility that IL-6 has neuronal or synaptic actions. Studies in in vitro and in vivo models confirmed this possibility and showed that IL-6 can regulate a number of important neuronal and synaptic functions including synaptic transmission and synaptic plasticity, an important cellular mechanism of memory and learning. Behavioral studies in animal models provided further evidence of an important role for IL-6 as a regulator of CNS pathways that are critical to cognitive function. This review summarizes studies that have lead to our current state of knowledge. In spite of the progress that has been made, there is a need for a greater understanding of the physiological and pathophysiological actions of IL-6 in the CNS, the mechanisms underlying these actions, conditions that induce production of IL-6 in the CNS and therapeutic strategies that could ameliorate or promote IL-6 actions. This article is part of a Special Issue entitled 'Neuroimmunology and Synaptic Function'.

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          Author and article information

          Journal
          Neuropharmacology
          Neuropharmacology
          Elsevier BV
          1873-7064
          0028-3908
          Sep 2015
          : 96
          : Pt A
          Affiliations
          [1 ] Molecular and Cellular Neuroscience Department, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. Electronic address: gruol@scripps.edu.
          Article
          S0028-3908(14)00398-0 NIHMS644784
          10.1016/j.neuropharm.2014.10.023
          4446251
          25445486
          393d4f7e-e51b-4aff-8f2d-b5fe6caa1ec1
          History

          Ca(2+),Cerebellum,Cognitive function,Glia,Hippocampus,JAK/STAT,MAPK,Memory,NMDA,Neurologic disorders

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