The kinetics of monazomycin-induced voltage-dependent conductance. II. Theory and a demonstration of a form of memory

The empirical differential equation that describes the kinetics of monazomycin-induced voltage-dependent conductance is derived using a standard chemical kinetic formulation and the assumption that monazomycin entry into and exit from the membrane is autocatalytic. The predicted form of gating currents is shown and numerical calculations for this process are made using a range of values for two unmeasured variables. A form of "memory" is then demonstrated, along with the ability of the theoretical equation to explain the nature of the memory.     

The molecule-group schema of memory: storage, recognition and retrieval

A new schema, the molecule-group schema, explains memory storage, recognition and retrieval. The schema consists of three postulates about molecular specificity, grouping, and diffusion. In the schema, the physical memory trace consists of a stable group of different kinds of highly specific molecules. The schema is intended to provide an alternative to the widely known synaptic-change schema, in which it is assumed that changes of synaptic efficacies constitute the memory trace. The new schema is used to develop a particular model of memory. In the model, recognition occurs when specific intracellular "endotransmitters" react with complementary "endoreceptors" in the same cell. Retrieval, modelled as the process whereby memory causes the recurrence of a previously experienced pattern of neural activity, occurs when a group of pools of endotransmitters, located within an intracellular memory organelle, is released, allowing the endotransmitters to diffuse to the periphery of the cell body. The model suffices to explain long-term and short-term memory of events as well as innate memory.     

The Astrocentric Hypothesis: proposed role of astrocytes in consciousness and memory formation.

Consciousness is self-awareness. This process is closely associated with attention and working memory, a special form of short-term memory, which is vital when solving explicit task. Edelman has equated consciousness as the "remembered present" to highlight the importance of this form of memory (G.M. Edelman, Bright Air, Brilliant Fire, Basic Books, New York, 1992). The majority of other memories are recollections of past events that are encoded, stored, and brought back into consciousness if appropriate for solving new problems. Encoding prior experiences into memories is based on the salience of each event (A.R. Damasio, Descartes' Error, G.P. Putnam's Sons, New York, 1994; G.M. Edelman, Bright Air, Brilliant Fire, Basic Books, New York, 1992). It is proposed that protoplasmic astrocytes bind attended sensory information into consciousness and store encoded memories. This conclusion is supported by research conducted by gliobiologist over the past 15 years.     

Hand-preference training in the mouse reveals key elements of its learning and memory process and resolves the phenotypic complexity in the behaviour.

Handedness in the mouse comprises 2 different behaviours. Some strains have a conditional behaviour, in that the mice learn a direction of hand preference in response to reaching for food, whereas other strains have an innate or constitutive behaviour, and prior experience has no measurable effect on their hand preference. However, hybrids from different strains have revealed both recessive and dominant forms of constitutive hand preference. We proposed that kinetic parameters of the learning process would resolve this genetic heterogeneity as well as the phenotypic complexity in the behaviour. We conducted and report here a detailed kinetic analysis of hand-preference training in the C57BL/6J strain. It revealed elements of the fundamental process of learning and long-term memory that underlies the behaviour by documenting consolidation of memory, blocking of this consolidation by an inhibitor of protein synthesis, retention of memory, and speed of learning in response to training reaches. Furthermore, speed of learning is clearly described by 2 parameters that we call "capacity" (or maximum amount of learned preference) and "ability" (or number of training reaches to achieve half the capacity). These 2 kinetic parameters can vary independently among genetically different strains that learn a preference, and we used them to demonstrate that the respective recessive and dominant forms of constitutive hand-preference may be the consequence of a true null or loss of function and a gain of function, possibly a memory regulator, in the learning process. The quantitative measures provide a sensitive and selective method to establish the fundamental learning process underlying mouse hand preference and to demonstrate empirically how genes and contextual environment shape its phenotypic complexity.     

An algebraic model of an associative noise-like coding memory

A mathematical model of an associative memory is presented, sharing with the optical holography memory systems the properties which establish an analogy with biological memory. This memory system-developed from Gabor's model of memoryis based on a noise-like coding of the information by which it realizes a distributed, damage-tolerant, equipotential storage through simultaneous state changes of discrete substratum elements. Each two associated items being stored are coded by each other by means of two noise-like patterns obtained from them through a randomizing preprocessing. The algebraic braic transformations operating the information storage and retrieval are matrix-vector products involving Toeplitz type matrices. Several noise-like coded memory traces are superimposed on a common substratum without crosstalk interference; moreover, extraneous noise added to these memory traces does not injure the stored information. The main performances shown by this memory model are: i) the selective, complete recovering of stored information from incomplete keys, both mixed with extraneous information and translated from the position learnt; ii) a dynamic recollection where the information just recovered acts as a new key for a sequential retrieval process; iii) context-dependent responses. The hypothesis that the information is stored in the nervous system through a noise-like coding is suggested. The model has been simulated on a digital computer using bidimensional images.     

Functional neuroanatomy of the autobiographical memory

Autobiographical memory refers to events and information about personal life and the self. Within autobiographical memory, many authors make a difference between episodic and semantic components. Study of retrograde amnesia gives information about memory consolidation. According to the "standard model" of consolidation, the medial temporal lobe plays a time-limited role in retrieval memory. Functional neuroanatomy studies of autobiographical memory are very few and many are recent. These studies concern which brain regions are involved in the autobiographical retrieval, episodic or semantic autobiographical memory and consolidation process. Results show that autobiographical retrieval depends on specific brain regions like frontal cortex. Concerning memory consolidation, findings are most consistent with the idea that hippocampal complex is involved in both recent and remote memories.     

Extinction of a passive avoidance response of mice with a depressive-like state

The analysis of a behaviour and memory of mice with depressive state is conducted. The mice with "behavioral despair" obtained by forced swimming and mice with submissive stereotype generated by 20 confrontations were used. They were characterized by increased anxiety and reduced exploratory activity in tests of the elevated plus-maze and light/dark apparatus. It is shown that for want of behavioral differences in manifestation of a depressive state the process of extinction was opposite. Mice with "behavioral despair" revealed retention of a high level of memory trace retrieval down to the 21st day of testing reflecting essential delay of extinction. Submissive mice displayed fast extinction begining with the 5th day of testing.     

Iteration model of starch hydrolysis by amylolytic enzymes.

An elaborate computer program to simulate the process of starch hydrolysis by amylolytic enzymes was been developed. It is based on the Monte Carlo method and iteration kinetic model, which predict productive and non-productive amylase complexes with substrates. It describes both multienzymatic and multisubstrate reactions simulating the "real" concentrations of all components versus the time of the depolymerization reaction the number of substrates, intermediate products, and final products are limited only by computer memory. In this work, it is assumed that the "proper" substrate for amylases is the glucoside linkages in starch molecules. Dynamic changes of substrate during the simulation adequately influence the increase or decrease of reaction velocity, as well as the kinetics of depolymerization. The presented kinetic model, can be adapted to describe most enzymatic degradations of a polymer. This computer program has been tested on experimental data obtained for alpha- and beta-amylases.     

Systems mechanisms of internal inhibition

The state of internal inhibition is analysed which is considered as a multifactor systemically organized process. On model of combined presentation of positive and inhibitory stimuli in experiments on white rats and dogs, a dependence is established of the efficiency of reinforcement cancellation factor on motivation intensity. Condition of negative emotion--frustration, "difficult state"-is a necessary link in the process of internal inhibition formation, since it is responsible for selection of non-reinforcement for storage in the long-term memory. Conclusion is made that active inhibition of goal-directed behaviour is mediated by actualization of memory trace, "engram of non-reinforcement" by negative conditioned stimulus.     

Total recall. Reconsolidation theory unifies cognitive psychology and neuroscience and creates new therapeutic options for memory-related disorders

New research reveals that long-term memory is not entirely stable and can be modified or potentially erased. These insights open new therapeutic possibilities for a range of memory-related diseases and disorders.There are many popular ideas about human memory serving as the repository of experiences etched into the substance of our brains until they are wiped out through death or disease. As the British writer Oscar Wilde put it, “Memory [...] is the diary that we all carry about with us.” And even if we sometimes cannot remember a particular event or person, we rarely doubt our memories. Friedrich Nietzsche, the German philosopher, placed great faith in memory, noting that, “The existence of forgetting has never been proved: we only know that some things don''t come to mind when we want them.”Despite these popular notions of infallible human memories, our understanding of how long-term memory works has changed dramatically during the past decade: it seems that our memories are not as permanent as we once thought. This has profound implications for both neuroscience and for treating a range of cognitive disorders including PTSD (post-traumatic stress disorder), drug addiction, chronic pain and even possibly Alzheimer disease....it seems that our memories are not as permanent as we once thoughtFor a long time, neurologists and psychiatrists had assumed that after an initial period of consolidation, during which memories are liable to change or be erased, memories eventually become enshrined and immune to alteration. But since 2000, this memory consolidation theory has gradually been replaced by a new one called reconsolidation, which posits that long-term memories can, at least in some circumstances, be changed. On activation or recall, the memory of an object or event enters an update process during which it can be strengthened, weakened or modified, just as short-term memories can be during the initial consolidation phase. The new reconsolidation theory has created great excitement among cognitive disorder researchers and practitioners. As many disorders are associated with some form of long-term memory malfunction or impairment, a reliable method that can reactivate and amend these memories would have great potential as a treatment; indeed a number of clinical trials to treat PTSD are currently testing this new understanding of memories.As many disorders are associated with some form of long-term memory malfunction or impairment, a reliable method that can reactivate and amend these memories would have great potential as a treatment...As happens so often in science, reconsolidation is actually an old idea that has been reincarnated. The theory first emerged in the 1960s when neurologists found that fear memories in rats could be greatly weakened if they were reactivated on recall (Misanin et al, 1968). Before then, it had been assumed that retrograde amnesia—the inability to access memories formed during or just before a traumatic event or illness—worked backwards in time to affect recently acquired memories. Retrograde amnesia also occurs in humans as a result of head injuries or, sometimes, extreme trauma. The experiments in rats, however, showed that even older memories might be vulnerable if they were in an active state of recall at the time of the trauma, but interest in the research waned because of the lack of any neurological or molecular basis for the theory. This all changed with the publication of a seminal paper in 2000 by Karim Nader at McGill University in Montreal, Canada, who demonstrated the reconsolidation of a fear memory in the lateral amygdala (Nader et al, 2000). This walnut-sized region in the medial temporal lobe of the brain has a key role in emotional memory in that it orchestrates the production of hormones or neurotransmitters such as dopamine, noradrenaline and adrenaline.Various forms of extinction training have long been applied to some disorders, notably PTSD...The work by Nader and Joseph LeDoux at New York University, USA, heralded the beginning of a unification between the previously largely distinct fields of neuroscience and cognitive psychology. Neuroscience had been driven chiefly by animal research to identify the underlying molecular, genetic and neurochemical basis of behaviour, emotion and memory. Cognitive psychology had been based almost entirely on behavioural experiments in humans. This unification process is still in its infancy, but advances in imaging techniques, particularly functional magnetic resonance imaging, promises to combine behavioural experiments in humans with observing changes in brain activity. According to Valérie Doyère, from the Centre of Neurosciences at Paris-Sud University in France, it will help resolve questions about how different regions of the brain interact during memory recall and reconsolidation. “I think the next step is to do neural imaging, as this would help detect at which step in the network the system has been modified or blocked,” Doyère, a pioneer of reconsolidation theory and collaborator of LeDoux and Nader, explained. “That is difficult to know unless you do have some way of analysing the neural network activity to try and see what you update and where.”Even without this insight, a lot of progress has been made in linking molecular events at the neuron level with the reconsolidation process—at least in animals. The starting point was the discovery by Nader and colleagues that reconsolidation in rats involved protein synthesis. They noted from other work that the initial consolidation of fear memories in rats could be inhibited by infusion of the protein synthesis inhibitor anisomycin into the amygdala, shortly after fear training. Such training typically involves traditional methods first used by the Russian physiologist Ivan Pavlov (1849–1936) in which an animal is given a so-called conditional stimulus (CS), such as a particular sound, followed shortly by an unconditional stimulus (US), such as an electric shock. The animal learns to associate the two so that exposure to the sound triggers fear: it begins with the activation of the amygdala, which is followed by a signalling cascade that leads to elevated heart and respiratory rates, with an associated increase in glucose production in preparation for the ''fight or flight'' response. The administration of anisomycin shortly after this training process blocks consolidation and prevents the animal from associating the CS signal with the US response.Similarly, Nader found that if the rats were exposed to the CS some days after the initial conditioning, to recall the association between the sound and the electric shock, anisomycin blocked reconsolidation and generated amnesia: the rats ''forgot'' the association between CS and US and had a greatly reduced fear response on exposure to the CS. Nader argued that this must mean the reconsolidation of the memory had been interrupted, because if the rats were given anisomycin after the initial training, but without exposure to the CS sound, they retained their fear conditioning. This link between memory reconsolidation and protein synthesis has also been demonstrated in other animals, including primitive invertebrates such as worms, suggesting that this is an evolutionarily conserved adaptation (Rose & Rankin, 2006).Attempts to observe this link between reconsolidation and protein synthesis in humans, however, have remained elusive. “We can''t test whether the mechanisms in humans are mediated by protein synthesis because those drugs would not be approved for human use,” Nader said. “Usually, rodent preps are used to understand the molecular mechanisms, and these seem to generalize to humans.”Indeed, Nader argues that evidence for reconsolidation in humans is now very strong in the light of recent work by LeDoux, demonstrating that the principles of fear extinction training in rats could be applied to humans to weaken the association between a CS trigger and memory of the US (Schiller et al, 2010). Human participants were shown an object and then given a mild electric shock in classical Pavlovian conditioning—the authors tested for the presence of the fear memory by measuring the change in skin electrical conductance in response to seeing the object. Once this fear memory was established, the authors reminded the participants of the object a day later to initiate the reconsolidation process, but then provided information that the same object was now ''safe''—this being called ''extinction training''. A day later, the participants were tested again to see whether the object elicited a fear response.The key point is that extinction training had to be conducted within the reconsolidation window, when the memory was temporarily unstable, to eliminate the fear response. The researchers also showed that rewriting the fear memory was specific to the CS object that was reactivated. If participants had been conditioned to associate several different objects with fear, then extinction training would only work on the specific object used during the training. Participants would continue to associate the other objects with fear, indicating that extinction training is selective.Various forms of extinction training have long been applied to some disorders, notably PTSD—an anxiety disorder that occurs in the aftermath of exposure to a traumatic experience involving death or the threat of death. The victim ingests a trauma memory that is emotionally overwhelming and cannot be resolved in the normal way, often intruding spontaneously into consciousness with a continued state of hypervigilance. The idea of extinction training is to force sufferers to actively recall memories frequently, but success has so far been mixed.The ability to stimulate memory could inspire new treatments for sufferers from memory loss...Although anisomycin cannot be given to PTSD sufferers to edit long-term memories, propranolol is an alternative. It has already been approved to treat hypertension as a so-called beta blocker that blocks the beta andrenergic receptor and diminishes the effect of stress hormones. Having been largely replaced by other drugs for treating high blood pressure, interest in propranolol was revived by its potential for treating PTSD in association with psychotherapy (Brunet et al, 2007). It also triggered research into the role of beta adrenergic receptors in PTSD, notably by Jacek Debiec and colleagues at New York University, who found that adrenergic signalling in the amygdala is involved in the memory consolidation process (Debiec et al, 2011).Drugs such as propranolol seem to suppress memory reconsolidation and thereby weaken the emotions associated with trauma memories. This is the theory, and early evidence of success has attracted significant interest in the USA, where PTSD is a particular problem given the country''s longstanding involvement in armed conflicts and the resulting large number of former soldiers suffering from the syndrome.The US Department of Defense''s standard treatment for PTSD has been cognitive behavioural therapy, in which individuals learn to identify thoughts that make them feel afraid or upset and then try to replace them with less distressing thoughts. But the potential of propanolol to replace or enhance cognitive behavioural therapy has prompted the US National Institutes of Health to conduct a phase II clinical trial, for which it is currently recruiting volunteers.The urgency of finding a more complete cure for PTSD has been increased by recent indications that the disorder not only diminishes quality of life for sufferers and their families, but also has serious long-term effects on physical as well as mental health, including premature ageing and a heightened risk of dementia. This link was confirmed by a recent retrospective study of 181,093 US war veterans aged 55 years or older, 53,155 of whom had PTSD (Yaffe et al, 2010). Kristine Yaffe (University of California, San Francisco and the San Francisco Veterans Affairs Medical Center) and her colleagues found that veterans with PTSD had a 10.6% risk of developing dementia compared with 6.6% among the general elderly population without PTSD. Although this result was statistically significant given that the study was adjusted for other factors such as demographic variation and psychiatric illnesses, it did not entirely preclude other risk factors. The causes of the higher risk of dementia were related to either the physiological stress on the brain with associated inflammation, or the systemic effect of long-term disruption to memory functioning, or probably a combination of both.The emphasis in treating PTSD and addictive disorders is on weakening aspects of long-term memory, but the emerging reconsolidation theory can equally provide clinical benefits by strengthening connections, as LeDoux pointed out. “Memory reconsolidation is not a process of weakening memory from the evolutionary point of view. It is an update mechanism. It allows memories to be changed when new information is available,” he said. “An extreme example from our work is that fear memory can be increased or decreased, depending on how you activate beta-adrenergic receptors. Block these during retrieval and you get a weakening of memory; stimulate these and you get an enhancement.” As happens so often in science, reconsolidation is actually an old idea that has been reincarnatedThe ability to stimulate memory could inspire new treatments for sufferers from memory loss, according to Doyère. “In the case of a disease like Alzheimer''s, it may be possible to reincorporate some elements and recover memory that has been lost. At least it may be possible to delay some of the symptoms,” she explained. Yet, more work is needed to expand on the emerging theory of reconsolidation, particularly in humans, because human memory recall goes beyond what happens in most animals. “Humans have the knowledge of a memory association and that may reactivate the emotional value,” Doyère commented. In other words, humans can better exploit their associated knowledge of events that they recall either wittingly or possibly in dreams, and this can affect the reconsolidation process. Moreover, there is also the role of sleep and dreaming in long-term memory recall and reconsolidation. In any case, it seems that reconsolidation as a unifying theory has both great therapeutic and scientific potential to explore human memory.     

Development and homeostasis of T cell memory in rhesus macaque.

The rhesus macaque (RM) is a critical animal model for studies of viral pathogenesis and immunity, yet fundamental aspects of their cellular immune response remain poorly defined. One such deficiency is the lack of validated phenotypic signatures for their naive and memory T cell subsets, and the resultant unavailability of accurate information on their memory T cell development, homeostasis, and function. In this study, we report a phenotypic paradigm allowing definitive characterization of these subsets and their comprehensive functional analysis. Naive T cells are optimally delineated by their homogeneous CD95(low)CD28(high)beta(7) integrin(int) (CD4+) or CD95(low)CD28(int)CD11a(low) (CD8+) phenotypes. This subset 1) was present in blood and secondary lymph tissues, but not effector sites; 2) vastly predominated in the fetal/neonatal immune system, but rapidly diminished with postnatal age; 3) lacked IFN-gamma production capability, and specific responses to RM CMV; and 4) demonstrated low in vivo proliferative activity. CD4+ and CD8+ memory subsets were CD95(high), but otherwise phenotypically heterogeneous and included all IFN-gamma production, RM CMV-specific responses, effector site T cells, and demonstrated high in vivo proliferative activity ( approximately 10 times the naive subset). These analyses also revealed the RM "effector memory" subset within the overall memory population. This population, best defined by lack of CD28 expression, contained the majority of RM CMV-specific cells, was highly enriched in extralymphoid effector sites, and comprised an increasing proportion of total memory cells with age. The effector memory subset demonstrated similar in vivo proliferative activity and survival as CD28+ "central memory" T cells, consistent with independent homeostatic regulation.     

Physical models of neural networks

The state of art in computer modelling of neural networks with associative memory is reviewed. The available experimental data are considered on learning and memory of small neural systems, on isolated synapses and on molecular level. Computer simulations demonstrate that realistic models of neural ensembles exhibit properties which can be interpreted as image recognition, categorization, learning, prototype forming, etc. A bilayer model of associative neural network is proposed. One layer corresponds to the short-term memory, the other one to the long-term memory. Patterns are stored in terms of the synaptic strength matrix. We have studied the relaxational dynamics of neurons firing and suppression within the short-term memory layer under the influence of the long-term memory layer. The interaction among the layers has found to create a number of novel stable states which are not the learning patterns. These synthetic patterns may consist of elements belonging to different non-intersecting learning patterns. Within the framework of a hypothesis of selective and definite coding of images in brain one can interpret the observed effect as the "idea? generating" process.     

T cell-mediated immunity to oncornavirus-induced tumors. I. Ly phenotype of precursor and effector cytolytic T lymphocytes

Regression of tumor induced by murine sarcoma virus (MSV) is accompanied by the formation of specific cytolytic T lymphocytes (CTL). Selection of T-cells sets by Ly phenotype determination allows separation of T sets involved in the cytolytic reaction. After MSV inoculation we demonstrate that a) Ly123+ cells contain precursors of CTL, b) direct cytolysis is mainly mediated by Ly23 cells, 3) cytolytic memory is divisible into "early" memory, carried by Ly23 cells, and "late" memory, which reverts to an Ly123 precursor population, and d) Ly1 cells are required to induce anti-MSV antibody formation.     

The transducer and encoder of frog muscle spindles are essentially nonlinear. Physiological conclusions from a white-noise analysis

1. Nonlinear second order white-noise analysis has been applied to the isolated frog muscle spindle. Power (²) of the Gaussian white noise (GWN) and the average prestretch level L were varied and the response of both the isolated receptor potential (transducer) and the action potential (encoder) level were analysed. 2. The standard white-noise method is briefly presented. Particular emphasis, however, is put on the limitations in the range of validity of the method and, consequently, on the use and interpretation of the kernels as a Wiener model. Conclusions in the present paper are within this frame and are mainly of qualitative nature. 3. The analysis reveals that the nonlinear contributions of the model are essential for approximating physiological results, thus ruling out purely linear modelling for this receptor organ. 4. The dependence of the transducer kernels on are compatible with the behaviour of a rectifier. Rectification is represented by the lack of hyperpolarization within the isolated receptor potential and is enhanced by the substantial memory in the linear and nonlinear kernels as demonstrated by their extent in time. This is equivalent to low power in high frequencies of the response. Obviously, the hyperpolarizing potentials following each spike counteract the long transducer memory. 5. At the encoder level the memory of the system is strongly reduced. This is achieved by using predominantly high frequency components of the receptor potential for triggering the process of impulse generation, and by the precise coupling and high frequency content of the impulses. This coupling precision is possible because of the sensitivity of the spike-generating mechanism to steep rising transients of the receptor potential and also owing to the reduction in transducer memory by the hyperpolarizing afferpotentials. 6. The preference given to the high frequency components is also read from the structure of the second order transducer kernel and from both the linear and the second order encoder kernels, which allows the most effective input waveform for triggering action potentials to be determined. 6. When the operating point is changed to higher prestretch values, kernel heights increase strongly implying higher response strength of the muscle spindle. The kernel structure is changed as well in the direction of reducing the effective memory already at the level of the receptor potentials, probably a means to prevent too high depolarization values.     

Structural drift: the population dynamics of sequential learning

We introduce a theory of sequential causal inference in which learners in a chain estimate a structural model from their upstream "teacher" and then pass samples from the model to their downstream "student". It extends the population dynamics of genetic drift, recasting Kimura's selectively neutral theory as a special case of a generalized drift process using structured populations with memory. We examine the diffusion and fixation properties of several drift processes and propose applications to learning, inference, and evolution. We also demonstrate how the organization of drift process space controls fidelity, facilitates innovations, and leads to information loss in sequential learning with and without memory.     

Oscillatory synchrony and human visual cognition.

Oscillatory synchrony could be used to establish dynamic links between the various cortical areas participating in the same cognitive process. Is it possible to detect oscillatory synchrony in humans, and is it relevant to behavior? There is now converging evidence for the existence of a transient oscillatory activity in the gamma range (30-60 Hz), obtained in response to static visual objects, and having only a loose temporal relationship to stimulus onset. This so-called "induced" gamma response is much larger in response to coherent static or moving objects. However, functional variations of gamma and/or beta (15-20 Hz) oscillations are not restricted to perceptive, bottom-up mechanisms, but are also observed during visual imagery or short-term memory maintenance. Oscillations at the scalp level thus seem to reflect large-scale neural cooperativity in a variety of task-dependent networks. Human intra-cranial recordings in a short-term memory paradigm further reveal the existence and the task-dependency of oscillatory synchrony in the beta range, between focal sites separated by several centimeters and with a few milliseconds time-lag. These findings thus confirm experimentally the hypothesis of a functional role of synchronized oscillatory activity in the coordination of distributed neural activity in humans, and support Hebb's concept of short-term memory maintenance by reentrant activity within the activated network. In addition, the intra-cranial data obtained in humans and monkeys also help to better understand the neural mechanisms generating scalp-recorded oscillations.     

Presenilin-1 and memories of the forebrain.

In this issue of Neuron, report that forebrain-specific Presenilin-1 conditional knockout mice show defects in enrichment-induced neurogenesis in the dentate gyrus. This defect in neurogenesis is associated with enhanced fear memory of contextual cues when animals are subjected to enrichment between training and testing. The authors suggest that neurogenesis in the adult dentate gyrus may serve to clear out old memory traces from the hippocampus, thus leaving the hippocampus available for new memory processing.     

From John McCain to Abu Ghraib: Tortured Bodies and Historical Unaccountability of U.S. Empire

ABSTRACT   John McCain, once considered a "friend" of Vietnam because of his support for normalized relations with the United States, has since lost his standing. Claims to inhumane treatment and torture while a prisoner in the "Hanoi Hilton" have met with angry denials and calls for more attention to the humanitarian care that McCain and others received. Recent U.S. allegations of human rights abuses in Vietnam following the Abu Ghraib prison scandal have further strained relations, as have charges leveled against Vietnamese small-scale producers of dishonest trade practices. Drawing on these exchanges, I examine competing representations of Vietnamese wartime acts that have permeated the "normalization" process. Neoliberal rhetorics aimed at "saving" the Vietnamese economy and its allegedly blemished human rights record are countered by discourses and images that lay claim to a Vietnamese "tradition" of wartime compassion and humanitarianism that also demands U.S. historical accountability for imperial violence and its aftermaths. [Keywords: neoliberalism, violence, human rights, Vietnam, historical memory]     

Cell molecular computer. VIII. Possible construction of a molecular memory in biological membranes and principle of minimum expenditures of free energy in recording information]

The principle of minimum expenditure of "price of action" [5] provides in the liquid cell membrane such operative memory which uses for recording information from any receptor (multidigit number) the transmission of an electron with the loss smaller than 250 mev. According to the hypothesis such memory is constructed from equal protein molecules and different lipid addresses for different receptors. It works on Brown collisions, weak interactions between the molecules and capture bonds controlled by MCC with a minimum expenditure of free energ- for the formation and breakage of bonds.     

Secondary IgG responses to type III pneumococcal polysaccharide. I. Kinetics and antigen requirements.

Mice primed with a thymus- (T)3 dependent form of Type III pneumococcal polysaccharide (S3), i.e., S3 coupled to sheep or horse erythrocytes (S3-RBC), produce S3-specific IgG antibody after secondary challenge with either the T-dependent (S3-RBC) or T-independent (S3) form of the antigen. The potential to produce IgG antibody after challenge with S3-RBC appears earlier after priming than the potential to produce IgG after challenge with S3, suggesting that different "memory" cells may be involved in the two responses. The "memory" cells were shown to be S3-specific since S3 had to be present on the carrier in order for priming to occur and carrier specificity was not required for elicitation of the secondary response by S3-RBC.