Spike timing-dependent plasticity under imbalanced excitation and inhibition reduces the complexity of neural activity

被引:2
|
作者
Park, Jihoon [1 ,2 ]
Kawai, Yuji [2 ]
Asada, Minoru [1 ,2 ,3 ,4 ]
机构
[1] Natl Inst Informat & Commun Technol, Ctr Informat & Neural Networks, Suita, Japan
[2] Osaka Univ, Inst Open & Transdisciplinary Res Initiat, Symbiot Intelligent Syst Res Ctr, Suita, Japan
[3] Chubu Univ, Chubu Univ Acad Emerging Sci, Ctr Math Sci & Artificial Intelligence, Kasugai, Japan
[4] Int Profess Univ Technol Osaka, Osaka, Japan
基金
日本科学技术振兴机构; 日本学术振兴会;
关键词
E; I balance; spiking neural network; complexity; information transmission; neuropsychiatric brain disorder; self-organization; AUTISM; MODEL; SCHIZOPHRENIA; BALANCE; EXCITATION/INHIBITION; INTERNEURONS; MECHANISMS; HYPOTHESIS; ENTROPY; NEURONS;
D O I
10.3389/fncom.2023.1169288
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Excitatory and inhibitory neurons are fundamental components of the brain, and healthy neural circuits are well balanced between excitation and inhibition (E/I balance). However, it is not clear how an E/I imbalance affects the self-organization of the network structure and function in general. In this study, we examined how locally altered E/I balance affects neural dynamics such as the connectivity by activity-dependent formation, the complexity (multiscale entropy) of neural activity, and information transmission. In our simulation, a spiking neural network model was used with the spike-timing dependent plasticity rule to explore the above neural dynamics. We controlled the number of inhibitory neurons and the inhibitory synaptic weights in a single neuron group out of multiple neuron groups. The results showed that a locally increased E/I ratio strengthens excitatory connections, reduces the complexity of neural activity, and decreases information transmission between neuron groups in response to an external input. Finally, we argued the relationship between our results and excessive connections and low complexity of brain activity in the neuropsychiatric brain disorders.
引用
收藏
页数:13
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