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首页> 外文期刊>Neuron >Compartmentalized Ca(2+) channel regulation at divergent mossy-fiber release sites underlies target cell-dependent plasticity.
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Compartmentalized Ca(2+) channel regulation at divergent mossy-fiber release sites underlies target cell-dependent plasticity.

机译：间隔的Ca（2+）通道调节在不同的长满苔藓的纤维释放位点基础的细胞依赖可塑性。

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摘要

Hippocampal mossy fibers (MFs) innervate CA3 targets via anatomically distinct presynaptic elements: MF boutons (MFBs) innervate pyramidal cells (PYRs), whereas filopodial extensions (Fils) of MFBs innervate st. lucidum interneurons (SLINs). Surprisingly, the same high-frequency stimulation (HFS) protocol induces presynaptically expressed LTP and LTD at PYR and SLIN inputs, respectively. This differential distribution of plasticity indicates that neighboring, functionally divergent presynaptic elements along the same axon serve as autonomous computational elements capable of modifying release independently. Indeed we report that HFS persistently depresses voltage-gated calcium channel (VGCC) function in Fil terminals, leaving MFB VGCCs unchanged despite similar contributions of N- and P/Q-type VGCCs to transmission at each terminal. Selective Fil VGCC depression results from HFS-induced mGluR7 activation leading to persistent P/Q-type VGCC inhibition. Thus, mGluR7 localization to MF-SLIN terminals and not MFBs allows for MF-SLIN LTD expression via depressed presynaptic VGCC function, whereas MF-PYR plasticity proceeds independently of VGCC alterations.
机译：海马苔藓纤维（MF）通过解剖学上不同的突触前元素来支配CA3靶点：MF钮扣（MFBs）支配锥体细胞（PYR），而MFB的丝状伸展（Fils）支配st。透明中神经元（SLIN）。令人惊讶的是，相同的高频刺激（HFS）协议分别在PYR和SLIN输入上诱导了突触前表达的LTP和LTD。这种可塑性的差异分布表明，沿着同一轴突的相邻，功能不同的突触前突触元件充当能够独立修改释放的自主计算元件。实际上，我们报道了HFS持续压低Fil终端的电压门控钙通道（VGCC）功能，尽管N型和P / Q型VGCC对每个终端传输的贡献相似，但MFB VGCC保持不变。 HFS诱导的mGluR7激活导致选择性的Fil VGCC抑制，从而导致持续的P / Q型VGCC抑制。因此，mGluR7定位到MF-SLIN端子而非MFB允许通过抑制的突触前VGCC功能表达MF-SLIN LTD，而MF-PYR可塑性独立于VGCC改变而进行。

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