LTP-Induced Long-Term Stabilization of Individual Nascent Dendritic Spines
LTP-Induced Long-Term Stabilization of Individual Nascent Dendritic Spines
复制标题
DOI：
10.1523/jneurosci.1404-12.2013
复制
发表时间：
2013-01-09
影响因子：
5.3
通讯作者：
Zito, Karen
中科院分区：
文献类型：
--
作者：
Hill, Travis C.;Zito, Karen
学习新任务与新树突棘的生长和稳定有关。我们研究了长时程增强（LTP），一个关键的细胞机制，认为是学习的基础，在回路可塑性过程中，在选择性稳定个别新的棘中发挥作用。使用双光子谷氨酸释放，我们刺激新生的大鼠海马CA1区神经元树突棘的模式，诱导LTP，然后监测脊髓的生存率，使用延时成像。值得注意的是，我们发现LTP诱导的刺激增加了个体新脊柱的长期存活率（>14小时）。活动诱导的新脊柱稳定需要NMDA受体激活，并且对诱导LTP的刺激具有特异性。此外，废除CaMKII结合到NMDA受体废除活动诱导的新的脊柱稳定。我们的研究结果首次表明，除了增强预先存在的突触的功效之外，LTP诱导的刺激还促进新生棘从短暂的短暂状态过渡到更长寿命的持久状态。
Learning new tasks has been associated with increased growth and stabilization of new dendritic spines. We examined whether long-term potentiation (LTP), a key cellular mechanism thought to underlie learning, plays a role in selective stabilization of individual new spines during circuit plasticity. Using two-photon glutamate uncaging, we stimulated nascent spines on dendrites of rat hippocampal CA1 neurons with patterns that induce LTP and then monitored spine survival rates using time-lapse imaging. Remarkably, we found that LTP-inducing stimuli increased the long-term survivorship (>14 h) of individual new spines. Activity-induced new spine stabilization required NMDA receptor activation and was specific for stimuli that induced LTP. Moreover, abrogating CaMKII binding to the NMDA receptor abolished activity-induced new spine stabilization. Our findings demonstrate for the first time that, in addition to enhancing the efficacy of preexisting synapses, LTP-inducing stimuli promote the transition of nascent spines from a short-lived, transient state to a longer-lived, persistent state.