سیستم ایمنی بدن و تثبیت حافظه: نقش برای سیتوکین IL-1β

Interleukin-1 beta (IL-1β), known to play a role in orchestrating the physiological and behavioral adjustments that occur during sickness, has also been shown to significantly influence memory consolidation. To support this assertion we present neurobiological evidence that the substrates for IL-1β to influence memory processing and neural plasticity exist. We then present behavioral evidence that central IL-1β administration and agents that induce central IL-1β activity impair the consolidation of memories that depend on the hippocampal formation but have no effect on the consolidation of hippocampal-independent memories. Further, we demonstrate that the impairments in hippocampal-dependent memory consolidation produced by agents that induce IL-1β activity are blocked by antagonizing the actions of IL-1β. Finally, we discuss these data in terms of their implications for a physiological role of IL-1β in memory consolidation processes and a potential role of IL-1β in producing memory impairments associated with stress, aging, Alzheimer's disease, and AIDS related dementia complex.