Kovalchuk Yury, Hanse Eric, Kafitz Karl W, Konnerth Arthur
Institut für Physiologie, Ludwig-Maximilians Universität München, 80336 München, Germany.
Science. 2002 Mar 1;295(5560):1729-34. doi: 10.1126/science.1067766.
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 Ca2+ 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.
脑源性神经营养因子(BDNF)和其他神经营养因子在长时程增强(LTP)中起着关键作用。先前的报道指出神经营养因子作用于突触前位点。通过对小鼠海马切片中的齿状颗粒细胞进行成像,我们在树突和棘中而非突触前位点鉴定出BDNF诱发的Ca2+瞬变。将微弱的突触刺激爆发与短暂的树突BDNF应用配对,可立即强烈诱导LTP。LTP的诱导需要激活突触后Ca2+通道和N-甲基-D-天冬氨酸受体,并且突触后Ca2+瞬变的阻断可阻止LTP的诱导。因此,我们的结果表明BDNF介导的LTP是在突触后诱导的。我们发现树突棘是BDNF快速诱发Ca2+信号传导的唯一突触位点,这支持了这一结论。