Inhibitory Plasticity Permits the Recruitment of CA2 Pyramidal Neurons by CA3.
Inhibitory Plasticity Permits the Recruitment of CA2 Pyramidal Neurons by CA3.
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DOI：
10.1523/eneuro.0049-15.2015
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发表时间：
2015-07
期刊：
影响因子：
3.4
通讯作者：
Chevaleyre V
中科院分区：
文献类型：
--
作者：
Nasrallah K;Piskorowski RA;Chevaleyre V
CA2区是海马记忆形成的重要区域。然而，CA2锥体神经元（PN）如何参与海马内的输入仍然不清楚。CA3和CA2之间的兴奋性传递被强烈抑制，并且不是可塑的。我们在小鼠中发现，不同的活动模式实际上可以增加CA3和CA2之间的兴奋性驱动。我们提供的证据表明，这种作用是由抑制性突触（iLTD）的长期抑制介导的，因为它是由相同的协议引起的，并具有相同的药理学。此外，我们发现，远端输入的净兴奋驱动也增加后，iLTD诱导。兴奋性驱动的去抑制增加足以使CA3输入诱发CA2 PN中的动作电位放电。因此，这些数据表明，输出的CA2 PN可以门控由独特的活动依赖性可塑性的抑制性神经元在CA2区。
Area CA2 is emerging as an important region for hippocampal memory formation. However, how CA2 pyramidal neurons (PNs) are engaged by intrahippocampal inputs remains unclear. Excitatory transmission between CA3 and CA2 is strongly inhibited and is not plastic. We show in mice that different patterns of activity can in fact increase the excitatory drive between CA3 and CA2. We provide evidence that this effect is mediated by a long-term depression at inhibitory synapses (iLTD), as it is evoked by the same protocols and shares the same pharmacology. In addition, we show that the net excitatory drive of distal inputs is also increased after iLTD induction. The disinhibitory increase in excitatory drive is sufficient to allow CA3 inputs to evoke action potential firing in CA2 PNs. Thus, these data reveal that the output of CA2 PNs can be gated by the unique activity-dependent plasticity of inhibitory neurons in area CA2.