Erasure Of Memory Research Articles

Breslau or Wrocław? The identity of the city in regards to the World War II in an autobiographical reflection

On the 1st September 1939 a German city Breslau was found 40 kilometers from the border with Poland and the first front lines. Nearly six years later, controlled by the Soviets, the city came under the "Polish administration” in the "Recovered Territories". The new authorities from the beginning virtually denied all the past of the city, began the exchange of population and the gradual erasure of multicultural memory; the heritage of the past recovery continues today. The main objective of this paper is to present the complexity of history through episodes of a city history. The analysis of texts and images, biographies of the inhabitants / immigrants / exiles of Breslau / Wrocław and the results of modern research facilitate the creation of a complex political, economic, social and cultural landscape, rewritten by historical events and resettlement actions. http://dx.doi.org/10.14195/1647-6336_13_5

Extinction of Learned Fear Induces Hippocampal Place Cell Remapping

The extinction of learned fear is a hippocampus-dependent process thought to embody new learning rather than erasure of the original fear memory, although it is unknown how these competing contextual memories are represented in the hippocampus. We previously demonstrated that contextual fear conditioning results in hippocampal place cell remapping and long-term stabilization of novel representations. Here we report that extinction learning also induces place cell remapping in C57BL/6 mice. Specifically, we observed cells that preferentially remapped during different stages of learning. While some cells remapped in both fear conditioning and extinction, others responded predominantly during extinction, which may serve to modify previous representations as well as encode new safe associations. Additionally, we found cells that remapped primarily during fear conditioning, which could facilitate reacquisition of the original fear association. Moreover, we also observed cells that were stable throughout learning, which may serve to encode the static aspects of the environment. The short-term remapping observed during extinction was not found in animals that did not undergo fear conditioning, or when extinction was conducted outside of the conditioning context. Finally, conditioning and extinction produced an increase in spike phase locking to the theta and gamma frequencies. However, the degree of remapping seen during conditioning and extinction only correlated with gamma synchronization. Our results suggest that the extinction learning is a complex process that involves both modification of pre-existing memories and formation of new ones, and these traces coexist within the same hippocampal representation.

Southeast Asia. Interactions with a violent past: Reading post-colonial landscapes in Cambodia, Laos and Vietnam Edited by Vatthana Pholsena and Oliver Tappe Singapore: NUS Press, 2013. Pp. 300. Maps, Tables, Plates, Notes, Bibliography, Index.

Interactions with a violent past: Reading post-colonial landscapes in Cambodia, Laos and Vietnam Edited by VATTHANA PHOLSENA and OLIVER TAPPE Singapore: NUS Press, 2013. Pp. 300. Maps, Tables, Plates, Notes, Bibliography, Index. doi: 10.1017/S0022463414000691 'When a memory is recalled like a car part from storage, there is no scientific certainty as to how it is put back, probably not as it was.' Norman M. Klein, The history of forgetting: Los Angeles and the erasure of memory (Verso, 1997). Echoing Klein's work Ian Baird explains, 'We need to see memories as experiences that are not simply recalled, but rather produced and reproduced over time, and entwined with agency, so that in the end people are not simply recalling past acts, but are considering past productions and reproductions of the past' (p. 243). Within academia, there is a substantial amount of work on collective memory, but very little on how conflict areas shape it. This collection of essays addresses the lacuna by looking at the fluid process of collective memory for those who live in the post-conflict landscapes of Cambodia, Laos, and Vietnam. Each essay provides details into the way that war-torn places become sites of memory, what Pierre Nora calls lieux de memoire. In this way, the collection provocatively showcases the symbiosis between people's identities and their war debris. Krisna Uk writes about artists and craftsmen who attribute new meanings and functions to war relics and their memories. The 70-year-old Cambodian funerary painter Keulagn Beuragn transforms horrifying memories of the bombing plane into aesthetic remembrances of those who died by it (pp. 223-8). Not only memories of the war, but war-riddled landscapes change in the post-conflict era. Vatthana Pholsena's account of Route 9 in southern Laos provides powerful descriptions of the lives of Sepon villagers who lived through the US war in Vietnam and its aftermath. Vietnamese soldiers and Royal Lao Army prisoners repaired the road in the postwar period, converting sites like a 'reeducation camp' where prisoners were tortured into an exhibition centre. Pholsena argues that beyond these governmental endeavours is a local social component. Villagers in Sepon see the reconstruction of the road as a marking of progress, civilisation, and development. In this way, they situate their own narrative within the road restoration 'in a historical timetable that followed their own recovery from the war' (p. 172). In her chapter on war debris in Vietnam, Christina Schwenkel writes about the international tourism that has developed for demilitarised zones (p. 149), but also notes the cultures that develop between 'professional' deminers and 'hobby' deminers who collect war debris at their own peril (p. 147). Here, people are not only redefining meaning with the war debris; in this example, war debris is part of the process in which people are redefining themselves. Perhaps one of the more physical and horrific examples of this comes from Susan Hammond's accounts of Agent Orange in Vietnam. The negligent manufacturing of the herbicide by US companies like Monsanto and Dow led to the devastation of thousands of people in addition to their ecology. …

Capturing the Landauer bound through the application of a detailed Jarzynski equality for entropic memory erasure.

The states of an overdamped Brownian particle confined in a two-dimensional bilobal enclosure are considered to correspond to two binary values: 0 (left lobe) and 1 (right lobe). An ensemble of such particles represents bits of entropic information. An external bias is applied on the particles, equally distributed in two lobes, to drive them to a particular lobe erasing one kind of bit of information. It has been shown that the average work done for the entropic memory erasure process approaches the Landauer bound for a very slow erasure cycle. Furthermore, the detailed Jarzynski equality holds to a very good extent for the erasure protocol, so that the Landauer bound may be calculated irrespective of the time period of the erasure cycle in terms of the effective free-energy change for the process. The detailed Jarzynski equality applied to two subprocesses, namely the transition from entropic memory state 0 to state 1 and the transition from entropic memory state 1 to state 1, connects the work done on the system to the probability to occupy the two states under a time-reversed process. In the entire treatment, the work appears as a boundary effect of the physical confinement of the system not having a conventional potential energy barrier. Finally, an analytical derivation of the detailed and classical Jarzynski equality for Brownian movement in confined space with varying width has been proposed. Our analytical scheme supports the numerical simulations presented in this paper.

In vitro extinction learning in Hermissenda: involvement of conditioned inhibition molecules.

Extinction of a conditioned association is typically viewed as the establishment of new learning rather than the erasure of the original memory. However, recent research in the nudibranch, Hermissenda crassicornis (H.c.) demonstrated that extinction training (using repeated light-alone presentations) given 15 min, but not 23 h, after memory acquisition reversed both the cellular correlates of learning (enhanced Type B cell excitability) and the behavioral changes (reduced phototaxis) produced by associative conditioning (pairings of light, CS, and rotation, US). Here, we investigated the putative molecular signaling pathways that underlie this extinction in H.c. by using a novel in vitro protocol combined with pharmacological manipulations. After intact H.c. received either light-rotation pairings (Paired), random presentations of light and rotation (Random), or no stimulation (Untrained), B cells from isolated CNSs were recorded from during exposure to extinction training consisting of two series of 15 consecutive light-steps (LSs). When in vitro extinction was administered shortly (2 h, but not 24 h) after paired training, B cells from Paired animals showed progressive and robust declines in spike frequency by the 30th LS, while control cells (Random and Untrained) did not. We found that several molecules implicated in H.c. conditioned inhibitory (CI) learning, protein phosphatase 1 (PP1) and arachidonic acid (AA)/12-lipoxygenase (12-LOX) metabolites, also contributed to the spike frequency decreases produced by in vitro extinction. Protein phosphatase 2B (PP2B) also appeared to play a role. Calyculin A (PP1 inhibitor), cyclosporin A (PP2B inhibitor), and baicalein (a 12-LOX inhibitor) all blocked the spike frequency declines in Paired B cells produced by 30 LSs. Conversely, injection of catalytically-active PP1 (caPP1) or PP2B (caPP2B) into Untrained B cells partially mimicked the spike frequency declines observed in Paired cells, as did bath-applied AA, and occluded additional LS-produced reductions in spiking in Paired cells.

Maximum work extraction and implementation costs for nonequilibrium Maxwell's demons.

We determine the maximum amount of work extractable in finite time by a demon performing continuous measurements on a quadratic Hamiltonian system subjected to thermal fluctuations, in terms of the information extracted from the system. The maximum work demon is found to apply a high-gain continuous feedback involving a Kalman-Bucy estimate of the system state and operates in nonequilibrium. A simple and concrete electrical implementation of the feedback protocol is proposed, which allows for analytic expressions of the flows of energy, entropy, and information inside the demon. This let us show that any implementation of the demon must necessarily include an external power source, which we prove both from classical thermodynamics arguments and from a version of Landauer's memory erasure argument extended to nonequilibrium linear systems.

Chemical memory erasure; a photochemical model

Erasure of memory is an essential part of information processing. We consider a photochemical model to suggest a protocol for chemical memory erasure. It has been shown that successful erasure may be achieved by a synergy between a very weak but optimal thermal noise and a minuscule linear bias. The suggested scheme for photochemical transformation can be viewed as a chemical analogue of memory erasure procedure.

Depletion of perineuronal nets in the amygdala to enhance the erasure of drug memories.

Extinction therapy has been suggested to suppress the conditioned motivational effect of drug cues to prevent relapse. However, extinction forms a new inhibiting memory rather than erasing the original memory trace and drug memories invariably return. Perineuronal nets (PNNs) are a specialized extracellular matrix around interneurons in the brain that have been suggested to be a permissive factor that allows synaptic plasticity in the adolescent brain. The degradation of PNNs caused by chondroitinase ABC (ChABC) may generate induced juvenile-like plasticity (iPlasticity) and promote experience-dependent plasticity in the adult brain. In the present study, we investigated the effect of removing PNNs in the amygdala of rat on the extinction of drug memories. We found that extinction combined with intra-amygdala injections of ChABC (0.01 U/side) prevented the subsequent priming-induced reinstatement of morphine-induced and cocaine-induced, but not food -induced, conditioned place preference (CPP). Intra-amygdala injections of ChABC alone had no effect on the retention, retrieval, or relearning of morphine-induced CPP and storage of acquired food-induced CPP. Moreover, we found that the procedure facilitated the extinction of heroin- and cocaine-seeking behavior and prevented the spontaneous recovery and drug-induced reinstatement of heroin- and cocaine-seeking behavior. We also found that the effect of PNNs degradation combined with extinction may be mediated by the potentiation of several plasticity-related proteins in the amygdala. Altogether, our findings demonstrate that a combination of extinction training with PNNs degradation in the amygdala erases drug memories and suggest that ChABC may be an attractive candidate for the prevention of relapse.

Combination of fluoxetine and extinction treatments forms a unique synaptic protein profile that correlates with long-term fear reduction in adult mice

The antidepressant fluoxetine induces synaptic plasticity in the visual and fear networks and promotes the structural remodeling of neuronal circuits, which is critical for experience-dependent plasticity in response to an environmental stimulus. We recently demonstrated that chronic fluoxetine administration together with extinction training in adult mice reduced fear in a context-independent manner. Fear conditioning and extinction alter excitatory and inhibitory transmissions within the fear circuitry. In this study, we investigated whether fluoxetine, extinction or their combination produced distinct long-lasting changes in the synaptic protein profile in the amygdala, hippocampus and prefrontal cortex of conditioned mice. We determined that extinction induced synaptophysin expression and down-regulated the GluA1:GluA2 ratio throughout the fear network in water- and fluoxetine-treated mice, suggesting a common fluoxetine-independent mechanism for increased synaptic transmission and re-arrangement of AMPA-receptors by extinction training. In contrast to common changes, the presynaptic vesicular neurotransmitter transporters VGAT and Vglut1 were upregulated after extinction in water- and fluoxetine-treated mice, respectively. The cortical levels of the GABA transporter Gat1 were reduced in high-freezing water-drinking mice, suggesting a maladaptive increase of GABA spillover at cortical inhibitory synapses. Fear conditioning decreased, and extinction induced the expression of GABA-receptor alpha1 and alpha2 subunits in water- and fluoxetine-treated mice, respectively. Only a combination of fluoxetine with extinction enhanced GluN2A expression in the amygdala and hippocampus, emphasizing the role of this NMDA-receptor subunit in the successful erasure of fear memories. Our finding provides novel data that may become helpful in developing beneficial pharmacological fear-reducing treatment strategies.

Memory enhancement and erasure

Memory enhancement and erasure

Serotonin-related pathways and developmental plasticity: relevance for psychiatric disorders

Risk for adult psychiatric disorders is partially determined by early-life alterations occurring during neural circuit formation and maturation. In this perspective, recent data show that the serotonin system regulates key cellular processes involved in the construction of cortical circuits. Translational data for rodents indicate that early-life serotonin dysregulation leads to a wide range of behavioral alterations, ranging from stress-related phenotypes to social deficits. Studies in humans have revealed that serotonin-related genetic variants interact with early-life stress to regulate stress-induced cortisol responsiveness and activate the neural circuits involved in mood and anxiety disorders. Emerging data demonstrate that early-life adversity induces epigenetic modifications in serotonin-related genes. Finally, recent findings reveal that selective serotonin reuptake inhibitors can reinstate juvenile-like forms of neural plasticity, thus allowing the erasure of long-lasting fear memories. These approaches are providing new insights on the biological mechanisms and clinical application of antidepressants.

Entropic memory erasure.

We have considered a Brownian particle confined in a two-dimensional bilobal enclosure where the state of the particle represents a bit of information having binary value 0 (left lobe) or 1 (right lobe). A time linear force is applied on the particle, driving it selectively to a particular lobe, and thus erasing one bit of information. We explore the statistics of heat and work associated with memory erasure to realize the Landauer limit in the entropic domain. Our results suggest that the mean value of work done associated with the complete erasure procedure satisfies the Landauer bound even when the memory is purely entropic in nature.

A new direction in political sociology?

This essay reviews works in (political) sociology that offer alternatives to sociology-as-usual. Sociologists with even fleeting awareness of the recent history of political sociology are surely familiar with the cultural turn, the global turn, and the turn toward complexity; however, another turn seems to be afoot, one toward existential concerns that direct us to recover how people experience ‘the complex contradictions of the social and political world’ (Taylor, The New Political Sociology, p. 197). Complex experiences often leave behind residues or ‘traces,’ and contributors in a recently edited volume challenge sociologists to unlock the social significance of these traces and find new ways to capture what our methods capture so poorly, namely, popular forgettings, geographies of exclusion, and the slow erasure of deeds, memories, and other subjugated knowledges belonging to individuals who find themselves dismissed, dispelled, or disenfranchised by nation-states. Traces left behind by individuals navigating the complexities of contemporary experiments in human ‘being’ are just the sort of analysis that must, in principle, place the actor at the center of analysis, and, after careful study, we now appreciate that despite the analytical ease of assuming that actors are singular, sociologists should examine actors as plural and unearth their essential multiplicity.

The Debt of Memory: Reparations, Imagination, and History in Toni Morrison’s Beloved

essay focuses Toni Morrison's groundbreaking novel Beloved and examines issue of reparations in economic, affective, and historical terms. Beloved, I claim, addresses these debts via fiction by delving into recesses of traumatic memory. Debt is overriding metaphor of our time, a quintessential^ modernizing state and activity that weaves inequalities into fabric and practice of capital. To incur debt is to enter into an interpolative arrangement in which capital confers recognition through repetitive consumption. Morrison's novel redirects our contemporary dependence and understanding of debt from a tangible economic figure or amount to a cumulative colonial deficit spanning space and time of slavery. In this sense, contemporary economic debt functions as a recurring sign in longue duree of racial history, which calls for layered forms of reparations. When Morrison states, at end of novel, This is not a story to pass on ( 1987,274), she asks reader to confront debt assumed by traumas of slavery to enable us to transform this inheritance into a beloved future. To pass this story down is to forge a new repository of memory upon which a severely incurred debt-mnemonic, social, and material-can begin to be defrayed. Therefore fiction, for Morrison, compels reader to reimagine a concealed past as a reparative starting point, which not only summons ghastly foundations of Americas but in so doing, initiates conversations surrounding what was lost, established, and still owed.Indeed, idea of reparations has seen various iterations since end of slavery. Not only did President Lincoln favor some sort of reparations for newly freed slaves but several decades later, in 1915, Cornelius J. Jones brought a lawsuit demanding sixty-eight million dollars in reparative compensation for unpaid slave labor. In 1944 Gunnar Myrdal, Swedish economist and Nobel laureate, in his book An American Dilemma: The Negro Problem and Modern Democracy, argued for parcels of former plantations to be made available to ex-slaves through manageable, longterm installment plans. The call for reparations continued in 1960s, when activist James Forman, in his controversial Black Manifesto, boldly proposed five hundred million dollars in damages. Moreover, in 1972, in The Case for Black Reparations, Yale Law School professor Boris Bittker asserted that a history of race-based discrimination from slavery to Jim Crow, spanning over three centuries, caused undue social and economic injury to African Americans and suggested creation of a program to distribute resources to America's descendants of slaves. Finally, in a more recent text, The Debt: What America Owes to Blacks, Randall Robinson makes case for a national economic response that would effectively close the yawning gap between blacks and whites (Robinson 2000, 204).1 However, Robinson's argument marks a shift from a reductive, if necessary and just, economic discussion to a more wide-ranging cultural, historic, and psychic understanding of debt.2As he argues: But only slavery, with its sadistic patience, asphyxiated memory, and smothered cultures, has hulled empty a whole race of people with inter-generational efficiency. Every artifact of victims' past cultures, every custom, every ritual, every god, every language, every trace element of a people's whole heredity identity, wrenched from them and ground into a sharpe choking dust. It is a human rights crime without parallel in modern world. For it produces its victims ad infinitum, long after active statge of crime has ended (Robinson 2000, 216). In absence of economic reparations, Robinson proposes a black renaissance (237-47), a dynamic return to knowledge, memory, and creativity as a formula to halt production of victims generated by aftereffects of slavery and colonialism. Thus, Robinson compels reader to confront varying dimensions of debt as, one hand, virulent conjunction of economic processes-centuries of forced and unpaid labor-and other, imposed erasure of memory and culture. …

Demons: Maxwell's demon, Szilard's engine and Landauer's erasure–dissipation

This talk addressed the following questions in the public debate at HoTPI: (i) energy dissipation limits of switches, memories and control; (ii) whether reversible computers are possible, or does their concept violate thermodynamics; (iii) Szilard's engine, Maxwell's demon and Landauer's principle: corrections to their exposition in the literature; (iv) whether Landauer's erasure–dissipation principle is valid, if the same energy dissipation holds for writing information, or if it is invalid; and (v) whether (non-secure) erasure of memories, or the writing of the same amount of information, dissipates most heat.

An introduction to the Bioscience Birthday Symposium held in honour of Ole Petersen CBE, FRS

An introduction to the Bioscience Birthday Symposium held in honour of Ole Petersen CBE, FRS

Long-term memory mechanisms maintenance by protein kinase Mξ——a research progress

Background Long-term potentiation (LTP),as a classical electrophysiological models of neural plasticity and learning and memory mechanism,has been widely studied.The molecular mechanism underlying the induction of LTP has been identified,but it remains unknown the maintenance of memory storge.Protein kinase Mξ (PKMξ) is an autonomously active,atypical protein kinase C isoform which is necessary for maintaining LTP and long-term memory.Objective To summarize the recent research progress of the mechanisms of long-term memory maintained by PKMξ.Content This review elabrated the summary of PKMξ,molecular mechanism of memory storage,memory erasure and related diseases.Trend More in-depth researches will be carried out about the effects and possible mechanisms of PKMξ in maintaining the long-term memory. Key words: Protein kinase Mξ; Long-term potentiation; Long-term memory

The MAP(K) of fear: From memory consolidation to memory extinction

The highly conserved mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling cascade is involved in several intracellular processes ranging from cell differentiation to proliferation, as well as in synaptic plasticity. In the last two decades, the role of MAPK/ERK in long-term memory formation in mammals, particularly in fear-related memories, has been extensively investigated. In this review we describe knowledge advancement on the role of MAPK/ERK in orchestrating the intracellular processes that lead to the consolidation, reconsolidation and extinction of fear memories. In doing so, we report studies in which the specific role of MAP/ERK in switching from memory formation to memory erasure has been suggested. The possibility to target MAPK/ERK in developing and/or refining pharmacological approaches to treat psychiatric disorders in which fear regulation is defective has also been envisaged.

Calcium regulation of neural rhythms, memory and Alzheimer's disease.

Alzheimer's disease (AD) begins with a decline in cognition followed by neuronal cell death and dementia. These changes have been linked to a deregulation of Ca(2+) signalling caused by a progressive increase in the resting level of Ca(2+), which may influence cognition by interfering with the rhythm rheostat that controls the sleep/wake cycle. The rise in resting levels of Ca(2+) may not alter the processes of memory acquisition during consciousness (gamma and theta rhythms), but may duplicate some of the events that occur during the slow oscillations responsible for the twin processes of memory consolidation and memory erasure that occur during sleep. The persistent elevation in the resting level of Ca(2+) induced by an accumulation of amyloid β (Aβ) oligomers duplicates a similar small global elevation normally restricted to the period of slow oscillations when memories are erased during sleep. In AD, such a rapid erasure of memories soon after they are acquired during the wake period means that they are not retained for consolidation during sleep. The Aβ deregulates Ca(2+) signalling through direct effects on the neurons and indirectly by inducing inflammatory responses in the microglia and astrocytes. Some of these deleterious effects of Aβ may be alleviated by vitamin D.

Reelin, an extracellular matrix protein linked to early onset psychiatric diseases, drives postnatal development of the prefrontal cortex via GluN2B-NMDARs and the mTOR pathway

Defective brain extracellular matrix (ECM) is a factor of vulnerability in various psychiatric diseases such as schizophrenia, depression and autism. The glycoprotein reelin is an essential building block of the brain ECM that modulates neuronal development and participates to the functions of adult central synapses. The reelin gene (RELN) is a strong candidate in psychiatric diseases of early onset, but its synaptic and behavioral functions in juvenile brain circuits remain unresolved. Here, we found that in juvenile reelin-haploinsufficient heterozygous reeler mice (HRM), abnormal fear memory erasure is concomitant to reduced dendritic spine density and anomalous long-term potentiation in the prefrontal cortex. In juvenile HRM, a single in vivo injection with ketamine or Ro25-6981 to inhibit GluN2B-N-methyl-𝒟-aspartate receptors (NMDARs) restored normal spine density, synaptic plasticity and converted fear memory to an erasure-resilient state typical of adult rodents. The functional and behavioral rescue by ketamine was prevented by rapamycin, an inhibitor of the mammalian target of rapamycin pathway. Finally, we show that fear memory erasure persists until adolescence in HRM and that a single exposure to ketamine during the juvenile period reinstates normal fear memory in adolescent mice. Our results show that reelin is essential for successful structural, functional and behavioral development of juvenile prefrontal circuits and that this developmental period provides a critical window for therapeutic rehabilitation with GluN2B-NMDAR antagonists.