Humeau Yann, Lüthi Andreas
Friedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, CH-4058 Basel, Switzerland.
Neuropharmacology. 2007 Jan;52(1):234-43. doi: 10.1016/j.neuropharm.2006.07.010. Epub 2006 Aug 4.
Postsynaptic induction of long-term potentiation (LTP) at cortical and thalamic afferent synapses onto lateral amygdala (LA) projection neurons not only involves NMDA receptor activation, but also depends on L-type voltage-dependent calcium channels (L-VDCCs). Here we show, using whole cell recordings and two-photon Ca2+ imaging, that L-VDCCs contribute to the induction of dendritic Ca2+ spikes in LA projection neurons. Dendritic Ca2+ spikes can be induced in the absence of sodium spikes by supra-threshold somatic depolarization or by pairing sub-threshold depolarization with synaptic stimulation. Moreover, synaptic induction of Ca2+ spikes is facilitated by R-VDCCs in a pathway-specific manner. Once induced, dendritic Ca2+ spikes propagate into large parts of the dendritic tree. We show that pairing synaptic stimulation with single dendritic Ca2+ spikes can induce bi-directional plasticity, the sign of which might be determined by the anatomical location of active synaptic inputs relative to the spike initiation zone. These data suggest an important role for dendritic Ca2+ spikes in dendritic integration and provide a mechanism by which local synaptic activity may influence global dendritic integration in LA projection neurons.
在投射至外侧杏仁核(LA)投射神经元的皮质和丘脑传入突触上,突触后长时程增强(LTP)的诱导不仅涉及N-甲基-D-天冬氨酸(NMDA)受体激活,还依赖于L型电压依赖性钙通道(L-VDCCs)。在这里,我们使用全细胞记录和双光子Ca2+成像表明,L-VDCCs有助于LA投射神经元中树突状Ca2+尖峰的诱导。树突状Ca2+尖峰可通过阈上体细胞去极化或通过将阈下去极化与突触刺激配对,在无钠尖峰的情况下诱导产生。此外,R-VDCCs以通路特异性方式促进Ca2+尖峰的突触诱导。一旦被诱导,树突状Ca2+尖峰就会传播到树突树的大部分区域。我们表明,将突触刺激与单个树突状Ca2+尖峰配对可诱导双向可塑性,其信号可能由活跃突触输入相对于尖峰起始区的解剖位置决定。这些数据表明树突状Ca2+尖峰在树突整合中具有重要作用,并提供了一种机制,通过该机制局部突触活动可能影响LA投射神经元中的整体树突整合。