Pandey Anurag, Sikdar Sujit Kumar
Molecular Biophysics Unit, Indian Institute of Science, Bangalore, 560 012, India.
Molecular Biophysics Unit, Indian Institute of Science, Bangalore, 560 012, India
J Physiol. 2014 Aug 15;592(16):3537-57. doi: 10.1113/jphysiol.2014.273367. Epub 2014 Jun 6.
The subiculum is a structure that forms a bridge between the hippocampus and the entorhinal cortex (EC), and plays a major role in the memory consolidation process. Here, we demonstrate spike-timing-dependent plasticity (STDP) at the proximal excitatory inputs on the subicular pyramidal neurons of juvenile rat. Causal (positive) pairing of a single EPSP with a single back-propagating action potential (bAP) after a time interval of 10 ms (+10 ms) failed to induce plasticity. However, increasing the number of bAPs in a burst to three, at two different frequencies of 50 Hz (bAP burst) and 150 Hz, induced long-term depression (LTD) after a time interval of +10 ms in both the regular-firing (RF), and the weak burst firing (WBF) neurons. The LTD amplitude decreased with increasing time interval between the EPSP and the bAP burst. Reversing the order of the pairing of the EPSP and the bAP burst induced LTP at a time interval of -10 ms. This finding is in contrast with reports at other synapses, wherein pre- before postsynaptic (causal) pairing induced LTP and vice versa. Our results reaffirm the earlier observations that the relative timing of the pre- and postsynaptic activities can lead to multiple types of plasticity profiles. The induction of timing-dependent LTD (t-LTD) was dependent on postsynaptic calcium change via NMDA receptors in the WBF neurons, while it was independent of postsynaptic calcium change, but required active L-type calcium channels in the RF neurons. Thus the mechanism of synaptic plasticity may vary within a hippocampal subfield depending on the postsynaptic neuron involved. This study also reports a novel mechanism of LTD induction, where L-type calcium channels are involved in a presynaptically induced synaptic plasticity. The findings may have strong implications in the memory consolidation process owing to the central role of the subiculum and LTD in this process.
海马下脚是在海马体和内嗅皮质（EC）之间形成桥梁的一种结构，在记忆巩固过程中起主要作用。在此，我们证明了幼年大鼠海马下脚锥体神经元近端兴奋性输入处的尖峰时间依赖性可塑性（STDP）。单个兴奋性突触后电位（EPSP）与单个反向传播动作电位（bAP）在10毫秒（+10毫秒）的时间间隔后进行因果（正向）配对未能诱导可塑性。然而，将爆发中的bAP数量增加到三个，以50赫兹（bAP爆发）和150赫兹这两种不同频率，在+10毫秒的时间间隔后，在规则发放（RF）神经元和弱爆发发放（WBF）神经元中均诱导出了长期抑制（LTD）。LTD幅度随着EPSP与bAP爆发之间时间间隔的增加而减小。颠倒EPSP与bAP爆发的配对顺序在 -10毫秒的时间间隔诱导出了长时程增强（LTP）。这一发现与其他突触处的报道相反，在其他突触中，突触前 - 突触后（因果）配对诱导LTP，反之亦然。我们的结果再次证实了早期的观察结果，即突触前和突触后活动的相对时间可导致多种类型的可塑性模式。时间依赖性LTD（t-LTD）的诱导在WBF神经元中依赖于通过NMDA受体的突触后钙变化，而在RF神经元中它独立于突触后钙变化，但需要活性L型钙通道。因此，突触可塑性机制可能在海马亚区内因所涉及的突触后神经元而异。本研究还报道了一种新的LTD诱导机制，其中L型钙通道参与了突触前诱导的突触可塑性。由于海马下脚和LTD在这一过程中的核心作用，这些发现可能对记忆巩固过程具有重要意义。
