Synaptic plasticity in the absence of backpropagating spikes of layer II inputs to layer V pyramidal cells in rat visual cortex
Synaptic plasticity in the absence of backpropagating spikes of layer II inputs to layer V pyramidal cells in rat visual cortex
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DOI：
10.1111/j.1460-9568.2005.04094.x
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发表时间：
2005-05-01
影响因子：
3.4
通讯作者：
Singer, W
中科院分区：
文献类型：
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作者：
Stiefel, KM;Tennigkeit, F;Singer, W
突触传递的依赖于使用的变化被认为依赖于对突触前和突触后兴奋活动之间的时间相关性的评估。以往的研究表明，在突触前兴奋性输入与突触后去极化重合配对后，层V层锥体细胞出现长时程增强(LTP)，从而诱发反向传播动作电位(BAPS)。在这里，我们将兴奋性II层输入与躯体超极化配对，它阻断了大鼠视皮层V层锥体细胞中的BAPS，并诱导了可靠的长期抑郁(LTD)。在胆碱能受体激活的基础上，这种不依赖BAP的方案也能诱导LTP，LTP不依赖N-甲基-D-天冬氨酸受体的激活，但可被代谢性谷氨酸受体(MGluR)拮抗剂阻断。
Use-dependent changes of synaptic transmission are thought to depend on the evaluation of temporal correlations between pre- and postsynaptic excitatory activity. Previous studies have demonstrated long-term potentiation (LTP) in layer V pyramidal cells after coincident pairing of presynaptic excitatory input with postsynaptic depolarizations, evoking backpropagating action potentials (BAPs). Here we paired excitatory layer II input with somatic hyperpolarization, which blocked BAPs in layer V pyramidal cells of rat visual cortex and induced reliable long-term depression (LTD). Upon cholinergic receptor activation, this BAP-independent protocol also induced LTP, which was not dependent on N-methyl-D-aspartate receptor activation, but blocked by metabotropic glutamate receptor (mGluR) antagonists.