Long-Term Information Storage by the Interaction of Synaptic and Structural Plasticity

2017 ◽  
pp. 343-360
Author(s):  
Michael Fauth ◽  
Florentin Wörgötter ◽  
Christian Tetzlaff
Keyword(s):  
Structural Plasticity ◽  
Information Storage

MODERN PROBLEMATICS AND ANALYSIS OF EFFICIENCY OF APPLICATION OF DIFFERENT APPROACHES TO DESTRUCTION OF INFORMATION ON MAGNETIC MEDIA

2019 ◽  
Vol 2 (12) ◽  
pp. 154-164
Author(s):  
O. Semenenko ◽  
O. Vodchyts ◽  
V. Koverga ◽  
R. Lukash ◽  
O. Lutsenko
Keyword(s):  
Armed Forces ◽  
Information Storage ◽  
Storage Device ◽  
Magnetic Media ◽  
Long Term Storage ◽  
Physical Impact ◽  
And Storage ◽  
Term Storage

The introduction and active use of information transmission and storage systems in the Ministry of Defense (MoD) of Ukraine form the need to develop ways of guaranteed removal of data from media after their use or long-term storage. Such a task is an essential component of the functioning of any information security system. The article analyzes the problems of guaranteed destruction of information on magnetic media. An overview of approaches to the guaranteed destruction of information on magnetic media of different types is presented, and partial estimates of the effectiveness of their application are given by some generally accepted indicators of performance evaluation. The article also describes the classification of methods of destruction of information depending on the influence on its medium. The results of the analysis revealed the main problems of application of software methods and methods of demagnetization of the information carrier. The issue of guaranteed destruction of information from modern SSD devices, which are actively used in the formation of new systems of information accumulation and processing, became particularly relevant in the article. In today's conditions of development of the Armed Forces of Ukraine, methods of mechanical and thermal destruction are more commonly used today. In the medium term, the vector of the use of information elimination methods will change towards the methods of physical impact by the pulsed magnetic field and the software methods that allow to store the information storage device, but this today requires specialists to develop new ways of protecting information in order to avoid its leakage.

scholarly journals An Endogenous RNA Transcript Antisense to CNGα1 Cation Channel mRNA

2002 ◽  
Vol 13 (10) ◽  
pp. 3696-3705 ◽  
Author(s):  
Chin-Hung Cheng ◽  
David Tai-Wai Yew ◽  
Hiu-Yee Kwan ◽  
Qing Zhou ◽  
Yu Huang ◽  
...  
Keyword(s):  
Expression System ◽  
Expression Patterns ◽  
Long Term Potentiation ◽  
Information Storage ◽  
Term Potentiation ◽  
Hippocampal Ca1 ◽  
Oocyte Expression System ◽  
Neuronal Functions ◽  
Rna Transcript

CNG channels are cyclic nucleotide-gated Ca2+-permeable channels that are suggested to be involved in the activity-dependent alterations of synaptic strength that are thought to underlie information storage in the CNS. In this study, we isolated an endogenous RNA transcript antisense to CNGα1 mRNA. This transcript was capable of down-regulating the expression of sense CNGα1 in theXenopus oocyte expression system. RT-PCR, Northern blot, and in situ hybridization analyses showed that the transcript was coexpressed with CNGα1 mRNA in many regions of human brain, notably in those regions that were involved in long-term potentiation and long-term depression, such as hippocampal CA1 and CA3, dentate gyrus, and cerebellar Purkinje layer. Comparison of expression patterns between adult and fetal cerebral cortex revealed that there were concurrent developmental changes in the expression levels of anti-CNG1 and CNGα1. Treatment of human glioma cell T98 with thyroid hormone T3 caused a significant increase in anti-CNG1 expression and a parallel decrease in sense CNGα1 expression. These data suggest that the suppression of CNGα1 expression by anti-CNG1 may play an important role in neuronal functions, especially in synaptic plasticity and cortical development. Endogenous antisense RNA-mediated regulation may represent a new mechanism through which the activity of ion channels can be regulated in the human CNS.

scholarly journals Molecular motor protein KIF5C mediates structural plasticity and long-term memory by constraining local translation

Cell Reports ◽  
2021 ◽  
Vol 36 (2) ◽  
pp. 109369
Author(s):  
Supriya Swarnkar ◽  
Yosef Avchalumov ◽  
Isabel Espadas ◽  
Eddie Grinman ◽  
Xin-an Liu ◽  
...  
Keyword(s):  
Molecular Motor ◽  
Motor Protein ◽  
Structural Plasticity ◽  
Long Term Memory ◽  
Local Translation ◽  
Term Memory

scholarly journals Nectin-3 modulates the structural plasticity of dentate granule cells and long-term memory

2017 ◽  
Vol 7 (9) ◽  
pp. e1228-e1228 ◽  
Author(s):  
X-X Wang ◽  
J-T Li ◽  
X-M Xie ◽  
Y Gu ◽  
T-M Si ◽  
...  
Keyword(s):  
Granule Cells ◽  
Structural Plasticity ◽  
Long Term Memory ◽  
Term Memory ◽  
Dentate Granule Cells

scholarly journals Non-ionotropic NMDA receptor signaling gates bidirectional structural plasticity of dendritic spines

2020 ◽  
Author(s):  
Ivar S. Stein ◽  
Deborah K. Park ◽  
Nicole Claiborne ◽  
Karen Zito
Keyword(s):  
Dendritic Spines ◽  
Structural Changes ◽  
Brain Plasticity ◽  
Structural Plasticity ◽  
Ion Flow ◽  
Neuronal Connections ◽  
Vital Component ◽  
Brain Circuit ◽  
Signaling Components

SUMMARYExperience-dependent refinement of neuronal connections is critically important for brain development and learning. Here we show that ion flow-independent NMDAR signaling is required for the long-term dendritic spine growth that is a vital component of brain circuit plasticity. We found that inhibition of p38 MAPK, shown to be downstream of non-ionotropic NMDAR signaling in LTD and spine shrinkage, blocked LTP-induced spine growth but not LTP. We hypothesized that non-ionotropic NMDAR signaling drives the cytoskeletal changes that support bidirectional spine structural plasticity. Indeed, we found that key signaling components downstream of non-ionotropic NMDAR function in LTD-induced spine shrinkage also are necessary for LTP-induced spine growth. Furthermore, NMDAR conformational signaling with coincident Ca2+ influx is sufficient to drive CaMKII-dependent long-term spine growth, even when Ca2+ is artificially driven through voltage-gated Ca2+ channels. Our results support a model in which non-ionotropic NMDAR signaling gates the bidirectional spine structural changes vital for brain plasticity.

scholarly journals Astrocytic microdomains from mouse cortex gain molecular control over long-term information storage and memory retention

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Beatrice Vignoli ◽  
Gabriele Sansevero ◽  
Manju Sasi ◽  
Roberto Rimondini ◽  
Robert Blum ◽  
...  
Keyword(s):  
Information Storage ◽  
Memory Retention ◽  
The Novel ◽  
Behavioral Test ◽  
Molecular Control ◽  
Mouse Cortex ◽  
Memory Circuits ◽  
Initial Activation ◽  
Synaptic Changes

AbstractMemory consolidation requires astrocytic microdomains for protein recycling; but whether this lays a mechanistic foundation for long-term information storage remains enigmatic. Here we demonstrate that persistent synaptic strengthening invited astrocytic microdomains to convert initially internalized (pro)-brain-derived neurotrophic factor (proBDNF) into active prodomain (BDNFpro) and mature BDNF (mBDNF) for synaptic re-use. While mBDNF activates TrkB, we uncovered a previously unsuspected function for the cleaved BDNFpro, which increases TrkB/SorCS2 receptor complex at post-synaptic sites. Astrocytic BDNFpro release reinforced TrkB phosphorylation to sustain long-term synaptic potentiation and to retain memory in the novel object recognition behavioral test. Thus, the switch from one inactive state to a multi-functional one of the proBDNF provides post-synaptic changes that survive the initial activation. This molecular asset confines local information storage in astrocytic microdomains to selectively support memory circuits.

scholarly journals Cyclase-associated protein 2 dimerization regulates cofilin in synaptic plasticity and Alzheimer's disease

2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Silvia Pelucchi ◽  
Lina Vandermeulen ◽  
Lara Pizzamiglio ◽  
Bahar Aksan ◽  
Jing Yan ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Actin Cytoskeleton ◽  
Structural Plasticity ◽  
Long Term Potentiation ◽  
Brain Diseases ◽  
Biological Trait ◽  
Term Potentiation ◽  
Cytoskeleton Dynamics

Abstract Regulation of actin cytoskeleton dynamics in dendritic spines is crucial for learning and memory formation. Hence, defects in the actin cytoskeleton pathways are a biological trait of several brain diseases, including Alzheimer's disease. Here, we describe a novel synaptic mechanism governed by the cyclase-associated protein 2, which is required for structural plasticity phenomena and completely disrupted in Alzheimer's disease. We report that the formation of cyclase-associated protein 2 dimers through its Cys32 is important for cyclase-associated protein 2 binding to cofilin and for actin turnover. The Cys32-dependent cyclase-associated protein 2 homodimerization and association to cofilin are triggered by long-term potentiation and are required for long-term potentiation-induced cofilin translocation into spines, spine remodelling and the potentiation of synaptic transmission. This mechanism is specifically affected in the hippocampus, but not in the superior frontal gyrus, of both Alzheimer's disease patients and APP/PS1 mice, where cyclase-associated protein 2 is down-regulated and cyclase-associated protein 2 dimer synaptic levels are reduced. Notably, cyclase-associated protein 2 levels in the cerebrospinal fluid are significantly increased in Alzheimer's disease patients but not in subjects affected by frontotemporal dementia. In Alzheimer's disease hippocampi, cofilin association to cyclase-associated protein 2 dimer/monomer is altered and cofilin is aberrantly localized in spines. Taken together, these results provide novel insights into structural plasticity mechanisms that are defective in Alzheimer's disease.

scholarly journals Gradation (approx. 10 size states) of synaptic strength by quantal addition of structural modules

2017 ◽  
Vol 372 (1715) ◽  
pp. 20160328 ◽  
Author(s):  
Kang K. L. Liu ◽  
Michael F. Hagan ◽  
John E. Lisman
Keyword(s):  
Functional Module ◽  
Late Phase ◽  
Matrix Material ◽  
Super Resolution ◽  
Long Term Potentiation ◽  
Information Storage ◽  
Homeostatic Plasticity ◽  
Memory Storage ◽  
Long Term Memory

Memory storage involves activity-dependent strengthening of synaptic transmission, a process termed long-term potentiation (LTP). The late phase of LTP is thought to encode long-term memory and involves structural processes that enlarge the synapse. Hence, understanding how synapse size is graded provides fundamental information about the information storage capability of synapses. Recent work using electron microscopy (EM) to quantify synapse dimensions has suggested that synapses may structurally encode as many as 26 functionally distinct states, which correspond to a series of proportionally spaced synapse sizes. Other recent evidence using super-resolution microscopy has revealed that synapses are composed of stereotyped nanoclusters of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors and scaffolding proteins; furthermore, synapse size varies linearly with the number of nanoclusters. Here we have sought to develop a model of synapse structure and growth that is consistent with both the EM and super-resolution data. We argue that synapses are composed of modules consisting of matrix material and potentially one nanocluster. LTP induction can add a trans-synaptic nanocluster to a module, thereby converting a silent module to an AMPA functional module. LTP can also add modules by a linear process, thereby producing an approximately 10-fold gradation in synapse size and strength. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.

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