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首页> 外文期刊>The European Journal of Neuroscience >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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Synaptic plasticity in the absence of backpropagating spikes of layer II inputs to layer V pyramidal cells in rat visual cortex.

机译:在没有向大鼠视皮层中的第V层锥体细胞输入的第II层反向传播尖峰的情况下,突触可塑性。

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摘要

Abstract 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.
机译:摘要突触传递的依赖于用途的变化被认为取决于对突触前和突触后兴奋活动之间的时间相关性的评估。先前的研究表明,在突触前兴奋性输入与突触后去极化同时配对,产生反向传播动作电位(BAP)后,V层锥体细胞中的长期增强(LTP)。在这里,我们将兴奋性第II层输入与体细胞超极化配对,后者阻止了大鼠视皮层V层锥体细胞中的BAP,并诱导了可靠的长期抑郁症(LTD)。胆碱能受体激活后,这种与BAP无关的方案也诱导了LTP,LTP不依赖于N-甲基-d-天冬氨酸受体的激活,但被代谢型谷氨酸受体(mGluR)拮抗剂阻断。

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