Postsynaptic induction of BDNF-mediated long-term potentiation
Postsynaptic induction of BDNF-mediated long-term potentiation
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DOI：
10.1126/science.1067766
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发表时间：
2002-03-01
期刊：
影响因子：
56.9
通讯作者：
Konnerth, A
中科院分区：
文献类型：
--
作者：
Kovalchuk, Y;Hanse, E;Konnerth, A
脑源性神经营养因子（BDNF）和其他神经营养因子与长时程增强（LTP）密切相关。先前的报道指出了神经营养因子作用的突触前位点。通过对小鼠海马切片中的齿状颗粒细胞成像，我们确定了树突和棘中BDNF诱发的Ca2+瞬变，但不在突触前位点。配对一个短暂的树突状脑源性神经营养因子的应用程序的突触刺激的弱爆发引起了立即和强大的诱导LTP。LTP诱导需要激活突触后Ca 2+通道和N-甲基-D-天冬氨酸受体，并通过阻断突触后Call瞬变来阻止。因此，我们的研究结果表明，BDNF介导的LTP诱导突触后。我们发现树突棘是快速BDNF诱发的Ca 2+信号传导的唯一突触位点，这一发现支持了这一结论。
Brain-derived neurotrophic factor (BDNF) and other neurotrophins are critically involved in long-term potentiation (LTP). Previous reports point to a presynaptic site of neurotrophin action. By imaging dentate granule cells in mouse hippocampal slices, we identified BDNF-evoked Ca2+ transients in dendrites and spines, but not at presynaptic sites. Pairing a weak burst of synaptic stimulation with a brief dendritic BDNF application caused an immediate and robust induction of LTP. LTP induction required activation of postsynaptic Ca2+ channels and N-methyl-D-aspartate receptors and was prevented by the blockage of postsynaptic Call transients. Thus, our results suggest that BDNF-mediated LTP is induced postsynaptically. Our finding that dendritic spines are the exclusive synaptic sites for rapid BDNF-evoked Ca2+ signaling supports this conclusion.