Exposure to music in the perinatal period enhances learning performance and alters BDNF/TrkB signaling in mice as adults
Exposure to music in the perinatal period enhances learning performance and alters BDNF/TrkB signaling in mice as adults
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DOI：
10.1016/j.bbr.2006.01.021
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发表时间：
2006-05-15
影响因子：
2.7
通讯作者：
Morita, Y
中科院分区：
文献类型：
--
作者：
Chikahisa, S;Sei, H;Morita, Y
音乐被认为对人类的各种表现都有有益的影响。然而，这种作用的生理和分子机制仍不清楚。我们研究了围产期音乐暴露对成年小鼠学习行为的影响，并测定了脑源性神经营养因子（BDNF）及其受体酪氨酸激酶受体B（Trk B）的水平，它们在突触可塑性中起关键作用。此外，我们测量了3-磷酸肌醇依赖性蛋白激酶-1（PDK 1）和丝裂原活化蛋白激酶（MAPK）的水平，这是BDNF/TrkB信号传导中两个主要途径的下游靶点。暴露于音乐的小鼠完成迷宫学习任务的错误比暴露于白色噪声的小鼠少，并且皮质中BDNF水平较低，TrkB和PDK 1水平较高。MAPK水平不变。此外，TrkB和PDK 1蛋白水平在皮层表现出显着的负相关性与错误的迷宫上的数量。这些结果表明，小鼠围产期暴露于音乐对BDNF/TrkB信号及其细胞内信号通路靶点（包括PDK 1）有影响，因此可能诱导改善学习和记忆功能。(C)2006 Elsevier B. V.保留所有权利。
Music has been suggested to have a beneficial effect on various types of performance in humans. However, the physiological and molecular mechanism of this effect remains unclear. We examined the effect of music exposure during the perinatal period on learning behavior in adult mice, and measured the levels of brain-derived neurotrophic factor (BDNF) and its receptor, tyrosine kinase receptor B (TrkB), which play critical roles in synaptic plasticity. In addition, we measured the levels of 3-phosphoinositide-dependent protein kinase-1 (PDK1) and mitogen-activated protein kinase (MAPK), downstream targets of two main pathways in BDNF/TrkB signaling. Music-exposed mice completed a maze learning task with fewer errors than the white noise-exposed mice and had lower levels of BDNF and higher levels of TrkB and PDK1 in the cortex. MAPK levels were unchanged. Furthermore, TrkB and PDK1 protein levels in the cortex showed a significant negative correlation with the number of errors on the maze. These results suggest that perinatal exposure of mice to music has an influence on BDNF/TrkB signaling and its intracellular signaling pathway targets, including PDK1, and thus may induce improved learning and memory functions. (C) 2006 Elsevier B.V. All rights reserved.