ACTIONS OF THE PRO-INFLAMMATORY CYTOKINE IL-1[beta] ON CENTRAL SYNAPTIC TRANSMISSION

Ellagic acid prevents cognitive and hippocampal long-term potentiation deficits and brain inflammation in rat with traumatic brain injury

“…Elevated levels of IL-1β cause memory impairment [23]. It has been suggested that three events affecting the magnitude of LTP, involving glutamate release modulation, the function of NMDARs and calcium channel influx can be influenced by IL-1β [45]. Our observations illustrated that inhibition of hippocampal LTP was associated with a significant increase in brain content of IL-1β (Fig.…”

Disease-associated amyloid and misfolded protein aggregates activate the inflammasome

“…Evidence for a potentially pathogenic role for IL-1b comes from its effects on long-term memory consolidation and cytotoxic influence on neuroendocrine cells. In the first case, IL-1b blocks hippocampal long-term potentiation (reviewed in [53]), whereas IL-1Ra might boost both shortand long-term memory functions [54]. As for cytotoxicity, IL-1b by itself might not directly kill neuronal cells, but there is interesting data to show that mixed cultures of neuronal and microglial cells could promote this effect via IL-1b [55].…”

Systemic lipopolysaccharide administration impairs retrieval of context–object discrimination, but not spatial, memory: Evidence for selective disruption of specific hippocampus-dependent memory functions during acute neuroinflammation

“…These pro-inflammatory cytokines have been demonstrated to directly affect neuronal function, including long-term potentiation (LTP), glutamate release, AMPA receptor trafficking, and activation of cell-signaling pathways (O'Connor and Coogan, 1999; Albensi and Mattson, 2000; D'Arcangelo et al, 2000; Tancredi et al, 2000; Vereker et al, 2000; Beattie et al, 2002; Lynch et al, 2004). Because these processes affect synaptic plasticity and neurotransmission, it is apparent that cytokines may impact neuronal processes pertinent to cognition.…”