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首页> 外文期刊>Brain, Behavior, and Immunity >Interleukin-1 beta-induced memory reconsolidation impairment is mediated by a reduction in glutamate release and zif268 expression and alpha-melanocyte-stimulating hormone prevented these effects
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Interleukin-1 beta-induced memory reconsolidation impairment is mediated by a reduction in glutamate release and zif268 expression and alpha-melanocyte-stimulating hormone prevented these effects

机译：白细胞介素-1β诱导的记忆重建障碍是由谷氨酸释放的减少和zif268表达的减少介导的，而α-黑素细胞刺激激素阻止了这些作用

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摘要

The immune system is an important modulator of learning, memory and neural plasticity. Interleukin 1 13 (IL-1 beta), a pro-inflammatory cytokine, significantly affects several cognitive processes. Previous studies by our group have demonstrated that intrahippocampal administration of IL-1 beta impairs reconsolidation of contextual fear memory. This effect was reversed by the melanocortin alpha-melanocyte-stimulating hormone (alpha-MSH). The mechanisms underlying the effect of IL-1 beta on memory reconsolidation have not yet been established. Therefore, we examined the effect of IL-1 beta on glutamate release, ERK phosphorylation and the activation of the transcription factor zinc finger- 268 (zif268) during reconsolidation. Our results demonstrated that IL-1 beta induced a significant decrease of glutamate release after reactivation of the fear memory and this effect was related to calcium concentration in hippocampal synaptosomes. IL-1 beta also reduced ERK phosphorylation and zif268 expression in the hippocampus. Central administration of a-MSH prevented the decrease in glutamate release, ERK phosphorylation and zif268 expression induced by IL-1 beta. Our results establish possible mechanisms involved in the detrimental effect of IL-1 beta on memory reconsolidation and also indicate that a-MSH may exert a beneficial modulatory role in preventing IL-1 beta effects. (C) 2015 Elsevier Inc. All rights reserved.
机译：免疫系统是学习，记忆和神经可塑性的重要调节剂。白细胞介素1 13（IL-1 beta）是一种促炎性细胞因子，可显着影响一些认知过程。我们小组先前的研究表明，海马内注射IL-1β会削弱背景恐惧记忆的巩固。黑素皮质素α-黑素细胞刺激激素（α-MSH）可逆转这种作用。尚未建立IL-1β对记忆整合的影响的机制。因此，我们在重新整合过程中检查了IL-1β对谷氨酸释放，ERK磷酸化和转录因子锌指268（zif268）活化的影响。我们的结果表明，在恐惧记忆重新激活后，IL-1β诱导了谷氨酸释放的显着降低，并且这种作用与海马突触体中的钙浓度有关。 IL-1β还减少了海马ERK磷酸化和zif268表达。中央管理a-MSH可防止IL-1β诱导的谷氨酸释放，ERK磷酸化和zif268表达的降低。我们的结果建立了可能的机制，参与了IL-1 beta对记忆重建的有害作用，并且还表明a-MSH可能在预防IL-1 beta的作用中发挥有益的调节作用。 （C）2015 Elsevier Inc.保留所有权利。

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