Memory rescue and learning in synaptic impaired neuronal circuits

被引:2
|
作者
Li, Kwan Tung [1 ,2 ]
Ji, Daoyun [3 ,4 ]
Zhou, Changsong [1 ]
机构
[1] Hong Kong Baptist Univ, Inst Computat & Theoret Studies, Beijing Hong Kong Singapore Joint Ctr Nonlinear &, Ctr Nonlinear Studies,Dept Phys, Hong Kong, Peoples R China
[2] Zhejiang Lab, Res Inst Artificial Intelligence, Res Ctr Augmented Intelligence, Hangzhou 311100, Peoples R China
[3] Baylor Coll Med, Dept Neurosci, Houston, TX 77030 USA
[4] Baylor Coll Med, Dept Mol & Cellular Biol, Houston, TX 77030 USA
基金
中国国家自然科学基金;
关键词
AMYLOID-BETA; WORKING-MEMORY; MOUSE MODEL; ALZHEIMERS-DISEASE; NMDA RECEPTORS; ENGRAM CELLS; PLASTICITY; CONNECTIVITY; DYSFUNCTION; MECHANISMS;
D O I
10.1016/j.isci.2023.106931
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Neuronal impairment is a characteristic of Alzheimer's disease (AD), but its effect on neural activity dynamics underlying memory deficits is unclear. Here, we stud-ied the effects of synaptic impairment on neural activities associated with mem-ory recall, memory rescue, and learning a new memory, in an integrate-and-fire neuronal network. Our results showed that reducing connectivity decreases the neuronal synchronization of memory neurons and impairs memory recall perfor-mance. Although, slow-gamma stimulation rescued memory recall and slow -gamma oscillations, the rescue caused a side effect of activating mixed memories. During the learning of a new memory, reducing connectivity caused impairment in storing the new memory, but did not affect previously stored memories. We also explored the effects of other types of impairments including neuronal loss and excitation-inhibition imbalance and the rescue by general increase of excit-ability. Our results reveal potential computational mechanisms underlying the memory deficits caused by impairment in AD.
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页数:22
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