Cell-specific, spike timing-dependent plasticities in the dorsal cochlear nucleus

被引:225
作者
Tzounopoulos, T
Kim, Y
Oertel, D
Trussell, LO
机构
[1] Oregon Hlth & Sci Univ, Oregon Hearing Res Ctr, Portland, OR 97239 USA
[2] Oregon Hlth & Sci Univ, Vollum Inst, Portland, OR 97239 USA
[3] Univ Wisconsin, Sch Med, Dept Physiol, Madison, WI 53706 USA
关键词
D O I
10.1038/nn1272
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
In the dorsal cochlear nucleus, long-term synaptic plasticity can be induced at the parallel fiber inputs that synapse onto both fusiform principal neurons and cartwheel feedforward inhibitory interneurons. Here we report that in mouse fusiform cells, spikes evoked 5 ms after parallel-fiber excitatory postsynaptic potentials (EPSPs) led to long-term potentiation (LTP), whereas spikes evoked 5 ms before EPSPs led to long-term depression (LTD) of the synapse. The EPSP-spike protocol led to LTD in cartwheel cells, but no synaptic changes resulted from the reverse sequence (spike-EPSP). Plasticity in fusiform and cartwheel cells therefore followed Hebbian and anti-Hebbian learning rules, respectively. Similarly, spikes generated by summing EPSPs from different groups of parallel fibers produced LTP in fusiform cells, and LTD in cartwheel cells. LTD could also be induced in glutamatergic inputs of cartwheel cells by pairing parallel-fiber EPSPs with depolarizing glycinergic PSPs from neighboring cartwheel cells. Thus, synaptic learning rules vary with the postsynaptic cell, and may require the interaction of different transmitter systems.
引用
收藏
页码:719 / 725
页数:7
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