TY - JOUR
T1 - Memory rescue and learning in synaptic impaired neuronal circuits
AU - Li, Kwan Tung
AU - Ji, Daoyun
AU - Zhou, Changsong
N1 - Funding Information:
This work was supported by STI 2030-Major Projects (2022ZD0208500), the National Natural Science Foundation of China, China (11975194), the Hong Kong Research Grant Council (GRF12200620), the Hong Kong Baptist University Research Committee Interdisciplinary Research Clusters Matching Scheme 2018/19 (RC-IRCMs/18-19/SCI01). This research was conducted using the resources of the High-Performance Computing Cluster Center at HKBU, which receives funding from the RGC and the HKBU.
Publisher Copyright:
© 2023 The Author(s).
PY - 2023/7/21
Y1 - 2023/7/21
N2 - Neuronal impairment is a characteristic of Alzheimer's disease (AD), but its effect on neural activity dynamics underlying memory deficits is unclear. Here, we studied the effects of synaptic impairment on neural activities associated with memory 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 performance. 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 excitability. Our results reveal potential computational mechanisms underlying the memory deficits caused by impairment in AD.
AB - Neuronal impairment is a characteristic of Alzheimer's disease (AD), but its effect on neural activity dynamics underlying memory deficits is unclear. Here, we studied the effects of synaptic impairment on neural activities associated with memory 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 performance. 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 excitability. Our results reveal potential computational mechanisms underlying the memory deficits caused by impairment in AD.
KW - Cognitive neuroscience
KW - Molecular neuroscience
KW - Neuroscience
UR - http://www.scopus.com/inward/record.url?scp=85161336258&partnerID=8YFLogxK
U2 - 10.1016/j.isci.2023.106931
DO - 10.1016/j.isci.2023.106931
M3 - Journal article
AN - SCOPUS:85161336258
SN - 2589-0042
VL - 26
JO - iScience
JF - iScience
IS - 7
M1 - 106931
ER -