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首页> 外文期刊>Neurobiology of learning and memory >Late expression of brain-derived neurotrophic factor in the amygdala is required for persistence of fear memory.
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Late expression of brain-derived neurotrophic factor in the amygdala is required for persistence of fear memory.

机译：杏仁核中脑源性神经营养因子的晚期表达对于持续恐惧记忆是必需的。

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摘要

In many instances, increase in neuronal activity can induce biphasic secretion of a modulator. The initial release of the modulator triggers the induction of synaptic plasticity, whereas the second-phase release reinforces the efficacy of synaptic transmission and growth of dendrites and axons. In this study, we showed that fear conditioning not only induced the first but also a second peak of brain-derived neurotrophic factor (BDNF) expression. Fluorescent immunohistostaining confirmed that BDNF expression increased at 1 and 12 h after conditioning and returned to baseline at 30 h after conditioning. Mature BDNF expression increased in a similar manner. TrkB-IgG or K252a infusion before training impaired fear memory on days 1 and 7 after training. In contrast, TrkB-IgG or K252a infusion 9 h after fear conditioning did not affect memory retention on day 1 after training but impaired fear memory on day 7 after training. Fear conditioning significantly enhanced Zif268 expression in the amygdala at 12 h after training; this enhanced expression was completely inhibited by TrkB-IgG infusion 9 h after training. The level of growth-associated protein 43 (GAP-43), a marker of newly formed synapses, in the amygdala increased 7 days after fear conditioning. Moreover, conditioned rats had higher AMPA/NMDA ratio than unpaired rats. These results suggest that consolidated memory could be continuously modulated by previous molecular changes produced during memory acquisition.
机译：在许多情况下，神经元活性的增加可诱导调节剂的双相分泌。调节剂的最初释放触发了突触可塑性的诱导，而第二阶段释放则增强了突触传递和树突和轴突生长的功效。在这项研究中，我们表明恐惧调节不仅诱发了脑源性神经营养因子（BDNF）表达的第一个高峰，而且还诱导了第二个高峰。荧光免疫组化证实BDNF表达在调理后1和12 h增加，并在调理后30 h返回基线。成熟的BDNF表达以类似的方式增加。训练前TrkB-IgG或K252a输注会在训练后第1天和第7天损害恐惧记忆。相比之下，恐惧调节后9小时的TrkB-IgG或K252a输注并不影响训练后第1天的记忆保持，但会损害训练后第7天的恐惧记忆。训练后12小时，恐惧条件显着增强杏仁核中Zif268的表达;训练后9小时，TrkB-IgG输注完全抑制了这种增强的表达。恐惧调节后7天，杏仁核中新形成的突触的标志物生长相关蛋白43（GAP-43）的水平增加。而且，条件大鼠比未配对的大鼠具有更高的AMPA / NMDA比。这些结果表明，合并的记忆可以通过记忆获取过程中先前产生的分子变化来连续调节。

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