当前位置: X-MOL 学术Neural Netw. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Simplified calcium signaling cascade for synaptic plasticity.
Neural Networks ( IF 7.8 ) Pub Date : 2019-12-02 , DOI: 10.1016/j.neunet.2019.11.022
Vladimir Kornijcuk 1 , Dohun Kim 2 , Guhyun Kim 2 , Doo Seok Jeong 1
Affiliation  

We propose a model for synaptic plasticity based on a calcium signaling cascade. The model simplifies the full signaling pathways from a calcium influx to the phosphorylation (potentiation) and dephosphorylation (depression) of glutamate receptors that are gated by fictive C1 and C2 catalysts, respectively. This model is based on tangible chemical reactions, including fictive catalysts, for long-term plasticity rather than the conceptual theories commonplace in various models, such as preset thresholds of calcium concentration. Our simplified model successfully reproduced the experimental synaptic plasticity induced by different protocols such as (i) a synchronous pairing protocol and (ii) correlated presynaptic and postsynaptic action potentials (APs). Further, the ocular dominance plasticity (or the experimental verification of the celebrated Bienenstock-Cooper-Munro theory) was reproduced by two model synapses that compete by means of back-propagating APs (bAPs). The key to this competition is synapse-specific bAPs with reference to bAP-boosting on the physiological grounds.

中文翻译:

简化的钙信号传导级联,用于突触可塑性。

我们提出了一个基于钙信号级联的突触可塑性模型。该模型简化了从钙流入到分别由假想的C1和C2催化剂控制的谷氨酸受体的磷酸化(增强)和去磷酸化(抑制)的完整信号传导途径。该模型基于有形的化学反应(包括虚拟催化剂)以实现长期可塑性,而不是各种模型中常见的概念性理论,例如预设的钙浓度阈值。我们的简化模型成功地再现了由不同协议(例如(i)同步配对协议和(ii)相关的突触前和突触后动作电位(AP))诱导的实验性突触可塑性。进一步,眼部支配性可塑性(或著名的Bienenstock-Cooper-Munro理论的实验验证)是由两个通过反向传播AP(bAP)竞争的模型突触复制而成的。竞争的关键是基于生理学上的增强bAP的突触特异性bAP。
更新日期:2019-12-02
down
wechat
bug