Differential BDNF signaling in dentate gyrus and perirhinal cortex during consolidation of recognition memory in the rat
Differential BDNF signaling in dentate gyrus and perirhinal cortex during consolidation of recognition memory in the rat
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DOI：
10.1002/hipo.22033
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发表时间：
2012-11-01
期刊：
影响因子：
3.5
通讯作者：
Kelly, Aine M.
中科院分区：
文献类型：
--
作者：
Callaghan, Charlotte K.;Kelly, Aine M.
长期记忆的巩固依赖于海马和相关皮质区域中新蛋白质的合成。神经营养因子脑源性神经营养因子（BDNF）受到活动依赖性细胞过程的严格调节，并与学习和记忆的基础机制密切相关。脑源性神经营养因子激活酪氨酸受体激酶（TrkB）可刺激与可塑性有关的细胞内信号级联反应，包括细胞外信号相关激酶（ERK）/促分裂原活化蛋白激酶（MAPK）途径和磷脂酰肌醇-3-激酶（PI 3 K）/Akt途径。本研究探讨了BDNF、ERK/MAPK和PI 3 K/AKT信号级联在大鼠再认记忆中的作用。我们报告说，再认记忆与齿状回和嗅周皮质BDNF的释放增加有关。这与齿状回中p44 ERK激活和c-fos表达以及嗅周皮质中PI 3 K激活和c-fos表达的显著增加有关。此外，识别记忆和相关的细胞信号转导事件在齿状回和嗅周皮层被阻断的Trk受体抑制剂tyrphostin AG 879的腹腔注射。这些数据与BDNF刺激的细胞内信号在大鼠识别记忆的巩固中起作用的假设是一致的。(c)2012 Wiley Periodicals，Inc.
Consolidation of long-term memory is dependent on synthesis of new proteins in the hippocampus and associated cortical regions. The neurotrophin brain-derived neurotrophic factor (BDNF) is tightly regulated by activity-dependent cellular processes and is strongly linked with mechanisms underlying learning and memory. BDNF activation of tyrosine receptor kinase (TrkB) stimulates intracellular signaling cascades implicated in plasticity, including the extracellular-signal related kinase (ERK)/mitogen-activated protein kinase (MAPK) pathway and the phosphatidylinositide-3-kinase (PI3K)/Akt pathway. Here, we investigate the role of BDNF, ERK/MAPK, and PI3K/AKT signaling cascade in recognition memory in the rat. We report that recognition memory was associated with increased release of BDNF in the dentate gyrus and perirhinal cortex. This was associated with significant increases in p44ERK activation and c-fos expression in the dentate gyrus and PI3K activation and c-fos expression in the perirhinal cortex. Furthermore, both recognition memory and the associated cell signaling events in dentate gyrus and perirhinal cortex were blocked by intraperitoneal injection of the Trk receptor inhibitor tyrphostin AG879. These data are consistent with the hypothesis that BDNF-stimulated intracellular signaling plays a role in consolidation of recognition memory in the rat. (c) 2012 Wiley Periodicals, Inc.