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CA1 锥体神经元的仿真模型揭示了在依赖于尖峰时间的突触可塑性过程中,钠离子/钙离子交换电流和钙离子激活的钾电流的作用相反。

Simulation model of CA1 pyramidal neurons reveal opposing roles for the Na+/Ca2+ exchange current and Ca2+-activated K+ current during spike-timing dependent synaptic plasticity.

机构信息

Department of Biological Sciences, The George Washington University, Washington DC, United States of America.

出版信息

PLoS One. 2020 Mar 9;15(3):e0230327. doi: 10.1371/journal.pone.0230327. eCollection 2020.

Abstract

Sodium Calcium exchanger (NCX) proteins utilize the electrochemical gradient of Na+ to generate Ca2+ efflux (forward mode) or influx (reverse mode). In mammals, there are three unique NCX encoding genes-NCX1, NCX2, and NCX3, that comprise the SLC8A family, and mRNA from all three exchangers is expressed in hippocampal pyramidal cells. Furthermore, mutant ncx2-/- and ncx3-/- mice have each been shown to exhibit altered long-term potentiation (LTP) in the hippocampal CA1 region due to delayed Ca2+ clearance after depolarization that alters synaptic transmission. In addition to the role of NCX at the synapse of hippocampal subfields required for LTP, the three NCX isoforms have also been shown to localize to the dendrite of hippocampal pyramidal cells. In the case of NCX1, it has been shown to localize throughout the basal and apical dendrite of CA1 neurons where it helps compartmentalize Ca2+ between dendritic shafts and spines. Given the role for NCX and calcium in synaptic plasticity, the capacity of NCX splice-forms to influence backpropagating action potentials has clear consequences for the induction of spike-timing dependent synaptic plasticity (STDP). To explore this, we examined the effect of NCX localization, density, and allosteric activation on forward and back propagating signals and, next employed a STDP paradigm to monitor the effect of NCX on plasticity using back propagating action potentials paired with EPSPs. From our simulation studies we identified a role for the sodium calcium exchange current in normalizing STDP, and demonstrate that NCX is required at the postsynaptic site for this response. We also screened other mechanisms in our model and identified a role for the Ca2+ activated K+ current at the postsynapse in producing STDP responses. Together, our data reveal opposing roles for the Na+/Ca2+ exchanger current and the Ca2+ activated K+ current in setting STDP.

摘要

钠钙交换器(NCX)蛋白利用 Na+ 的电化学梯度来产生 Ca2+ 外排(正向模式)或内流(反向模式)。在哺乳动物中,有三种独特的 NCX 编码基因-NCX1、NCX2 和 NCX3,它们构成了 SLC8A 家族,所有三种交换器的 mRNA 都在海马锥体细胞中表达。此外,已证明突变的 ncx2-/- 和 ncx3-/- 小鼠在海马 CA1 区均表现出长时程增强(LTP)改变,这是由于去极化后 Ca2+ 清除延迟改变了突触传递。除了 NCX 在海马亚区突触处对 LTP 的作用外,三种 NCX 同工型也已被证明定位于海马锥体细胞的树突。对于 NCX1,它已被证明定位于 CA1 神经元的基底和顶树突全长,在那里它有助于将 Ca2+ 分隔在树突干和棘突之间。鉴于 NCX 和钙在突触可塑性中的作用,NCX 剪接形式影响逆行动作电位的能力对诱导时程依赖的突触可塑性(STDP)有明显的影响。为了探索这一点,我们研究了 NCX 定位、密度和变构激活对前向和后向传播信号的影响,接下来采用 STDP 范式,使用逆行动作电位与 EPSP 配对来监测 NCX 对可塑性的影响。从我们的模拟研究中,我们确定了钠钙交换电流在使 STDP 正常化中的作用,并证明了 NCX 在突触后位点对此反应是必需的。我们还在模型中筛选了其他机制,并确定了突触后 Ca2+ 激活的 K+ 电流在产生 STDP 反应中的作用。总之,我们的数据揭示了钠钙交换器电流和 Ca2+ 激活的 K+ 电流在设定 STDP 中的相反作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/885d/7062500/81953752b30c/pone.0230327.g001.jpg

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