Zhang Yan-Ping, Holbro Niklaus, Oertner Thomas G
Friedrich Miescher Institute, Maulbeerstrasse 66, CH-4058 Basel, Switzerland.
Proc Natl Acad Sci U S A. 2008 Aug 19;105(33):12039-44. doi: 10.1073/pnas.0802940105. Epub 2008 Aug 12.
Long-term potentiation (LTP), a form of synaptic plasticity, is a primary experimental model for understanding learning and memory formation. Here, we use light-activated channelrhodopsin-2 (ChR2) as a tool to study the molecular events that occur in dendritic spines of CA1 pyramidal cells during LTP induction. Two-photon uncaging of MNI-glutamate allowed us to selectively activate excitatory synapses on optically identified spines while ChR2 provided independent control of postsynaptic depolarization by blue light. Pairing of these optical stimuli induced lasting increase of spine volume and triggered translocation of alphaCaMKII to the stimulated spines. No changes in alphaCaMKII concentration or cytoplasmic volume were observed in neighboring spines on the same dendrite, providing evidence that alphaCaMKII accumulation at postsynaptic sites is a synapse-specific memory trace of coincident activity.
长时程增强（LTP）是一种突触可塑性形式，是理解学习和记忆形成的主要实验模型。在此，我们使用光激活通道视紫红质-2（ChR2）作为工具，研究在LTP诱导过程中CA1锥体神经元树突棘中发生的分子事件。通过MNI-谷氨酸的双光子解笼，我们能够选择性地激活光学识别的棘突上的兴奋性突触，而ChR2则通过蓝光提供对突触后去极化的独立控制。这些光学刺激的配对诱导了棘突体积的持续增加，并触发了αCaMKII向受刺激棘突的转位。在同一树突上相邻的棘突中未观察到αCaMKII浓度或细胞质体积的变化，这证明αCaMKII在突触后位点的积累是同时活动的突触特异性记忆痕迹。
