A role for inflammatory mediators in the IL-18 mediated attenuation of LTP in the rat dentate gyrus

Elevated interleukin-18 serum levels in chronic schizophrenia: Association with psychopathology

“…IL-18 elevation contributes to both the central and peripheral stress response, and panic attacks in humans or restraint stress in mice induces a prompt increase in the level of circulating IL-18 (Kokai et al, 2002). Also, IL-18 is associated with other hallmarks of depression such as lethargy and loss of appetite and impaired learning and memory, which appears to be induced by attenuating long-term potentiation in hippocampal neurons (Cumiskey et al, 2007;Zorrilla et al, 2007). In addition, IL-18 is involved in sleep regulation (Kubota et al, 2001).…”

Neuroinflammatory changes negatively impact on LTP: A focus on IL-1β

“…Indeed the IL-18-induced attenuation of LTP in dentate gyrus in vitro and its ability to decrease NMDA receptor-mediated potentials were both blocked by IL-1ra, although the inhibitory effect of TNFα on LTP was unaffected (Curran and O'Connor, 2001). It was subsequently reported that the inhibitory effect of IL-18 on LTP could be attenuated by the mGluR5 specific antagonist MPEP and the group II mGluR antagonist, MTPG (Cumiskey et al, 2007c) and also by the COX-2 inhibitor, SC-236, the iNOS inhibitor 1400W and peroxisome proliferation activated receptor (PPAR)γ agonist, ciglitazone (Cumiskey et al, 2007b). Interestingly IL-18 also inhibits LTP of C-fiber-evoked field potentials induced by tetanic stimulation of the sciatic nerve in the spinal cord and the authors identified a key role for microglial activation since IL-18 was localized largely to microglia and this effect was inhibited by minocycline (Chu et al, 2012).…”

The link between inflammation, synaptic transmission and neurodegeneration in multiple sclerosis

“…[60][61][62][63] In particular, TNFa, IFNg and IL-1b are all potential candidates for such an action, as they are released in response to microglial activation, 49,50,64,65 increase in the CSF of MS patients, [66][67][68] and have been shown in vitro to enhance excitatory synaptic transmission 60,62,69 and downregulate…”