At the beginning of the 20^(th)century,German scientist Richard Semon introduced the term'engram'to describe the neural substrate implicated in the processes of memory formation and retrieval[1].The trace of t...At the beginning of the 20^(th)century,German scientist Richard Semon introduced the term'engram'to describe the neural substrate implicated in the processes of memory formation and retrieval[1].The trace of the corresponding biophysical and biochemical changes in the brain responding to an external stimulus is called an engram,and understanding the physical manifestations of memory formation and recall remains a fundamental yet unresolved question[2].展开更多
The curved martensite structures have been observed in CuZnAI-based shape memory alloys by both transmission electron microscope and optical microscope. It was found that the curved martensite structures observed in a...The curved martensite structures have been observed in CuZnAI-based shape memory alloys by both transmission electron microscope and optical microscope. It was found that the curved martensite structures observed in as-solution treated, as-aged and as-trained alloys usually occurred around dislocation tangles or precipitate, at the plate boundary or grain boundary, and when the growing plates collided with each other or alternate mutually.展开更多
Proper social behaviors are essential for survival and success,and deficits in these behaviors are associated with many brain disorders.However,the mechanisms underlying the formation and maintenance of social memory ...Proper social behaviors are essential for survival and success,and deficits in these behaviors are associated with many brain disorders.However,the mechanisms underlying the formation and maintenance of social memory remain poorly understood.In this study,we demonstrate that social interaction with unfamiliar mouse inducesα-andγ-secretase-dependent proteolysis of Neuroligin 1(NLG1)in the ventral hippocampus(vHPC).The intracellular hydrolysate fragment,NLG1-CTD,regulates synaptic plasticity,spine strengthening,and the maintenance of social memory through its PDZ binding domain(PBD)and the cofilin signaling pathway.Bothγ-secretase inhibition and deletion of the secretase recognition site on NLG1 prevent cofilin phosphorylation and impair the maintenance of social memory by inhibiting the production of NLG1-CTD.Injection of the Tat-PBD peptide into the vHPC inhibits cofilin activity and rescues deficits in social memory maintenance in mouse models.Additionally,our findings indicate that deficits in maintaining memory for sequentially presented social objects within a short temporal interval may be associated with insufficient levels of NLG1-CTD.Supplementation of Tat-PBD into the vHPC promotes maturation of dendritic spines and restores the maintenance of memory for the second social object.We also discovered that NLG1-CTD/PBD may play a role in maintaining novel object recognition memory.In summary,this work uncovers a novel mechanism that links extracellular and intracellular signal transduction processes to synaptic remodeling during learning and memory maintenance,providing a systematic perspective that connects memory formation,maintenance,and synaptic structural and functional plasticity.展开更多
文摘At the beginning of the 20^(th)century,German scientist Richard Semon introduced the term'engram'to describe the neural substrate implicated in the processes of memory formation and retrieval[1].The trace of the corresponding biophysical and biochemical changes in the brain responding to an external stimulus is called an engram,and understanding the physical manifestations of memory formation and recall remains a fundamental yet unresolved question[2].
基金Science Council of Shandong Province!under Grant No.89F0274
文摘The curved martensite structures have been observed in CuZnAI-based shape memory alloys by both transmission electron microscope and optical microscope. It was found that the curved martensite structures observed in as-solution treated, as-aged and as-trained alloys usually occurred around dislocation tangles or precipitate, at the plate boundary or grain boundary, and when the growing plates collided with each other or alternate mutually.
基金supported by grants from STI2030-Major Projects(2022ZD0205900,A.L.,2021ZD0204000,W.X.and A.L.)Natural Science Foundation of Jiangsu Province(BK20211561,A.L.)Natural Science Foundation of China(NSFC 32571220,A.L.)。
文摘Proper social behaviors are essential for survival and success,and deficits in these behaviors are associated with many brain disorders.However,the mechanisms underlying the formation and maintenance of social memory remain poorly understood.In this study,we demonstrate that social interaction with unfamiliar mouse inducesα-andγ-secretase-dependent proteolysis of Neuroligin 1(NLG1)in the ventral hippocampus(vHPC).The intracellular hydrolysate fragment,NLG1-CTD,regulates synaptic plasticity,spine strengthening,and the maintenance of social memory through its PDZ binding domain(PBD)and the cofilin signaling pathway.Bothγ-secretase inhibition and deletion of the secretase recognition site on NLG1 prevent cofilin phosphorylation and impair the maintenance of social memory by inhibiting the production of NLG1-CTD.Injection of the Tat-PBD peptide into the vHPC inhibits cofilin activity and rescues deficits in social memory maintenance in mouse models.Additionally,our findings indicate that deficits in maintaining memory for sequentially presented social objects within a short temporal interval may be associated with insufficient levels of NLG1-CTD.Supplementation of Tat-PBD into the vHPC promotes maturation of dendritic spines and restores the maintenance of memory for the second social object.We also discovered that NLG1-CTD/PBD may play a role in maintaining novel object recognition memory.In summary,this work uncovers a novel mechanism that links extracellular and intracellular signal transduction processes to synaptic remodeling during learning and memory maintenance,providing a systematic perspective that connects memory formation,maintenance,and synaptic structural and functional plasticity.
