A behavioural characterization of neonatal infection-facilitated memory impairment in adult rats
A behavioural characterization of neonatal infection-facilitated memory impairment in adult rats
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DOI：
10.1016/j.bbr.2005.12.002
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发表时间：
2006-04-25
影响因子：
2.7
通讯作者：
Maier, SF
中科院分区：
文献类型：
--
作者：
Bilbo, SD;Rudy, JW;Maier, SF
我们已经报道，在大鼠的新生期暴露在细菌(大肠杆菌)中与成年后对新环境的记忆受损有关。然而，只有在环境暴露后立即实施外周免疫挑战(细菌脂多糖)时，才会观察到损伤。目前这项研究的目标是更全面地描述这一现象。在实验1中，观察到幼年大鼠由于新生感染和随后的内毒素攻击而导致的记忆障碍，表明感染引起的变化发生在早期，然后表现在整个生命周期。在实验2中，幼年大鼠的感染没有导致成年后内毒素诱导的记忆障碍，这表明早期感染诱导的改变存在一个关键期。在实验3和实验4中，在新生感染的大鼠中，对新环境的记忆受到损害，这是一项依赖于海马体的任务，而对不依赖于海马体的音调的线索记忆没有受损。此外，无论是在条件化前24小时还是在条件化后24小时，作为新生感染的成年大鼠，无论是在条件化前24小时还是在条件化后24小时，长期而不是短期的上下文记忆都受到了损害。最后，在实验5中，没有观察到新生儿组在皮质酮或开阔场地行为上的差异，这表明减少冰冻到条件情境反映了记忆受损，而不仅仅是多动或应激反应改变。综上所述，我们已经证明，新生儿感染导致强大的海马体依赖的记忆损害，在成年后的免疫挑战使用了一些条件范式。(C)2005 Elsevier B.V.保留所有权利。
We have reported that exposure to bacteria (Escherichia coli) during the neonatal period in rats is associated with impaired memory for a novel context in adulthood. However, impairment is only observed if a peripheral immune challenge (bacterial lipopolysaccharide (LPS)) is administered immediately following context exposure. The goal of the current study was to more fully characterize this phenomenon. In Experiment 1, memory impairment as a result of neonatal infection and subsequent LPS challenge was observed in juvenile rats, indicating that the changes induced by infection occur early on and are then manifest throughout the lifespan. In Experiment 2, infection in juvenile rats did not lead to LPS-induced memory impairment in adulthood, suggesting there is a critical period for early infection-induced alterations. In Experiments 3 and 4, memory for a novel context was impaired in neonatally infected rats, a task that is dependent on the hippocampus, whereas cued memory for a tone, which does not depend on the hippocampus, was not impaired. Furthermore, long-term, but not short-term contextual memory was impaired in adult rats infected as neonates following an LPS challenge either 24 h before or immediately after conditioning. Finally, in Experiment 5, no neonatal group differences were observed in corticosterone or open field behaviour, suggesting that decreased freezing to a conditioned context reflects impaired memory, and not simply hyperactivity or altered stress reactivity. Taken together, we have demonstrated that neonatal infection results in robust hippocampal-dependent memory impairment following an immune challenge in adulthood using a number of conditioning paradigms. (C) 2005 Elsevier B.V. All rights reserved.