Wu Shengdun, Zhou Kang, Ai Yuping, Zhou Guanyu, Yao Dezhong, Guo Daqing
The Clinical Hospital of Chengdu Brain Science Institute, MOE Key Lab for NeuroInformation, Center for Information in Medicine, School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu, 611731 China.
Sichuan Institute for Brain Science and Brain-Inspired Intelligence, University of Electronic Science and Technology of China, Chengdu, 611731 China.
Cogn Neurodyn. 2021 Feb;15(1):53-64. doi: 10.1007/s11571-020-09578-6. Epub 2020 Mar 17.
Transient, task related synchronous activity within neural populations has been recognized as the substrate of temporal coding in the brain. The mechanisms underlying inducing and propagation of transient synchronous activity are still unknown, and we propose that short-term plasticity (STP) of neural circuits may serve as a supplemental mechanism therein. By computational modeling, we showed that short-term facilitation greatly increases the reactivation rate of population spikes and decreases the latency of response to reactivation stimuli in local recurrent neural networks. Meanwhile, the timing of population spike reactivation is controlled by the memory effect of STP, and it is mediated primarily by the facilitation time constant. Furthermore, we demonstrated that synaptic facilitation dramatically enhances synchrony propagation in feedforward neural networks and that response timing mediated by synaptic facilitation offers a scheme for information routing. In addition, we verified that synaptic strengthening of intralayer or interlayer coupling enhances synchrony propagation, and we verified that other factors such as the delay of synaptic transmission and the mode of synaptic connectivity are also involved in regulating synchronous activity propagation. Overall, our results highlight the functional role of STP in regulating the inducing and propagation of transient synchronous activity, and they may inspire testable hypotheses for future experimental studies.
神经群体内与任务相关的瞬态同步活动已被公认为大脑中时间编码的基础。瞬态同步活动的诱导和传播机制仍然未知，我们提出神经回路的短期可塑性（STP）可能是其中的一种补充机制。通过计算建模，我们表明短期易化极大地提高了群体尖峰的再激活率，并缩短了局部递归神经网络中对再激活刺激的反应潜伏期。同时，群体尖峰再激活的时间由STP的记忆效应控制，并且主要由易化时间常数介导。此外，我们证明了突触易化显著增强了前馈神经网络中的同步传播，并且由突触易化介导的反应时间提供了一种信息路由方案。此外，我们证实层内或层间耦合的突触增强会增强同步传播，并且我们证实突触传递延迟和突触连接模式等其他因素也参与调节同步活动传播。总体而言，我们的结果突出了STP在调节瞬态同步活动的诱导和传播中的功能作用，并且它们可能为未来的实验研究激发可检验的假设。
