Tzounopoulos Thanos, Rubio Maria E, Keen John E, Trussell Laurence O
Department of Cell Biology and Anatomy, Rosalind Franklin University, Chicago Medical School, North Chicago, IL 60064, USA.
Neuron. 2007 Apr 19;54(2):291-301. doi: 10.1016/j.neuron.2007.03.026.
Synapses may undergo long-term increases or decreases in synaptic strength dependent on critical differences in the timing between pre-and postsynaptic activity. Such spike-timing-dependent plasticity (STDP) follows rules that govern how patterns of neural activity induce changes in synaptic strength. Synaptic plasticity in the dorsal cochlear nucleus (DCN) follows Hebbian and anti-Hebbian patterns in a cell-specific manner. Here we show that these opposing responses to synaptic activity result from differential expression of two signaling pathways. Ca2+/calmodulin-dependent protein kinase II (CaMKII) signaling underlies Hebbian postsynaptic LTP in principal cells. By contrast, in interneurons, a temporally precise anti-Hebbian synaptic spike-timing rule results from the combined effects of postsynaptic CaMKII-dependent LTP and endocannabinoid-dependent presynaptic LTD. Cell specificity in the circuit arises from selective targeting of presynaptic CB1 receptors in different axonal terminals. Hence, pre- and postsynaptic sites of expression determine both the sign and timing requirements of long-term plasticity in interneurons.
突触强度可能会根据突触前和突触后活动时间的关键差异而经历长期增强或减弱。这种依赖于尖峰时间的可塑性（STDP）遵循支配神经活动模式如何诱导突触强度变化的规则。耳蜗背核（DCN）中的突触可塑性以细胞特异性方式遵循赫布和反赫布模式。在这里，我们表明，对突触活动的这些相反反应是由两条信号通路的差异表达引起的。Ca2+/钙调蛋白依赖性蛋白激酶II（CaMKII）信号传导是主细胞中赫布突触后长时程增强（LTP）的基础。相比之下，在中间神经元中，一种时间精确的反赫布突触尖峰时间规则是由突触后CaMKII依赖性LTP和内源性大麻素依赖性突触前长时程抑制（LTD）的联合作用产生的。回路中的细胞特异性源于不同轴突终末中突触前CB1受体的选择性靶向。因此，表达的突触前和突触后位点决定了中间神经元中长期可塑性的正负和时间要求。
