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PubMed2005

Differential developmental trajectories for egocentric, environmental and intrinsic frames of reference in spatial memory.

We studied the development of spatial frames of reference in children aged 3-6 years, who retrieved hidden toys from an array of identical containers bordered by landmarks under four conditions. By moving the child and/or the array between presentation and test, we varied the consistency of the hidden toy with (i) the body, and (ii) the testing room. The toy's position always remained consistent with (iii) the array and bordering landmarks. We found separate, additive performance advantages for consistency with body and room. These effects were already present at 3 years. A striking finding was that the room effect, which implies allocentric representations of the room and/or egocentric representations updated by self-motion, was much stronger in the youngest children than the body effect, which implies purely egocentric representations. Children as young as 3 years therefore had, and greatly favoured, spatial representations that were not purely egocentric. Viewpoint-independent recall based only on the array and bordering landmarks emerged at 5 years. There was no evidence that this later-developing ability, which implies object-referenced (intrinsic) representations, depended on verbal encodings. These findings indicate that core components of adult spatial competence, including parallel egocentric and nonegocentric representations of space, are present as early as 3 years. These are supplemented by later-developing object-referenced representations.

Child↗
PubMed2001

Differential effects of emotional content on event-related potentials in word recognition memory.

The aim of this study was to delineate the influence of the emotional content of stimuli to be remembered on the recognition performance of normal subjects by means of the event-related potential (ERP) technique. When words are presented repeatedly, brain responses to repeated and recognized items are characterized by a more positive waveform, referred to as "old/new effect". Words judged for their emotional connotation ("negative", "positive" and "neutral") were presented successively on a video monitor to subjects, who had the task to indicate whether a given word occurred for the first ("new") or second ("old") time within the list by pressing one of two buttons. For each word category, the ERPs of the old words were more positive compared to those of the new items from about 250 ms after stimulus. The old/new effect was significantly enhanced for the negative and positive items compared to the neutral stimuli between 450 and 650 ms after stimulus pointing to a significant influence of the emotional content of words on verbal memory processes. This paradigm appears to be feasible to investigate interactions of emotion and cognition in psychiatric patients.

Adult↗
PubMed2006

Differential CSF biomarker levels in APOE-epsilon4-positive and -negative patients with memory impairment.

OBJECTIVES: To investigate the relationships between episodic memory, APOE genotype, CSF markers (total tau, T-tau; phospho-tau, P-tau; beta-amyloid, Abeta42) and longitudinal cognitive decline. METHODS: 124 memory clinic patients were retrospectively divided into 6 groups based on (i) episodic memory function (Rey Auditory Verbal Learning Test, RAVLT): severe, moderate or no impairment (SIM, MIM or NIM), and (ii) APOE genotype (epsilon4+ or epsilon4-). CSF marker levels and cognitive decline were compared across groups. RESULTS: Episodic memory function, according to RAVLT scores, was significantly correlated with CSF marker levels only among epsilon4+ subjects and not among epsilon4- subjects. When comparing the 6 subgroups, SIM epsilon4+ and MIM epsilon4+ groups showed significantly lower Abeta42 levels than the other groups. T-tau and P-tau levels were significantly increased in SIM epsilon4+ when compared to all the other groups, including the SIM epsilon4- group. However, both SIM epsilon4+ and SIM epsilon4- declined cognitively during the follow-up. CONCLUSION: It remains to be determined whether APOE genotype affects the expression of biomarkers in CSF, or whether the different biomarker patterns reflect different types of disease processes in patients with progressive cognitive dysfunction.

Amyloid beta-Protein Precursor↗
PubMed1992

Differential effects of alprazolam and buspirone upon acquisition, retention, and retrieval processes in memory.

A group of 125 healthy young adults was given a memory battery 1 hour after administration of alprazolam (0.5 and 1.0 mg), buspirone (5 and 10 mg), and placebo under single-dose, double-blind conditions. On the wordlist recall battery and a 24-hour retest, alprazolam appeared to impair acquisition and retention in dosages of 1.0 mg; buspirone did not adversely affect test performance at either dosage. On the basis of a 3-stage model of memory, a neuroantomical/neurophysiological model is proposed to explain the selective effects of the benzodiazepines on memory function.

Adolescent↗
PubMed2002

Recruitment kinetics and composition of antibody-secreting cells within the central nervous system following viral encephalomyelitis.

Infection by the neurotropic JHM strain of mouse hepatitis virus produces an acute demyelinating encephalomyelitis. While cellular immunity initially eliminates infectious virus, CNS viral persistence is predominantly controlled by humoral immunity. To better understand the distinct phases of immune control within the CNS, the kinetics of humoral immune responses were determined in infected mice. Early during clearance of the JHM strain of mouse hepatitis virus, only few virus-specific Ab-secreting cells (ASC) were detected in the periphery or CNS, although mature B cells and ASC without viral specificity were recruited into the CNS concomitant with T cells. Serum antiviral Ab and CNS virus-specific ASC became prominent only during final elimination of infectious virus. Virus-specific ASC peaked in lymphoid organs before the CNS, suggesting peripheral B cell priming and maturation. Following elimination of infectious virus, virus-specific ASC continued to increase within the CNS and then remained stable during persistence, in contrast to declining T cell numbers. These data comprise three novel findings. Rapid recruitment of B cells in the absence of specific Ab secretion supports a potential Ab-independent effector function involving lysis of virus-infected cells. Delayed recruitment relative to viral clearance and subsequent maintenance of a stable CNS ASC population demonstrate differential regulation of T and B lymphocytes within the infected CNS. This supports a critical role of humoral immunity in regulating viral CNS persistence. Lastly, altered antiviral ASC specificities following clearance of infectious virus suggest ongoing recruitment of peripheral memory cells and/or local B cell differentiation.

Animals↗
PubMed2003

Differential role of mitogen-activated protein kinase in three distinct phases of memory for sensitization in Aplysia.

The mitogen-activated protein kinase (MAPK) pathway has been implicated recently in synaptic plasticity and memory. Here we used tail shock-induced sensitization of the tail-elicited siphon withdrawal reflex in Aplysia to examine the role of MAPK in three different phases of memory. We show that a specific pattern of serotonin (5-HT) application that produces intermediate-term and long-term synaptic facilitation (ITF and LTF, respectively) of the sensory-motor (SN-MN) synapses in Aplysia leads to sustained activation of extracellular signal-regulated kinase in the ventrocaudal cluster sensory neurons (SNs), which include the tail SNs. Furthermore, repeated tail shocks that induce intermediate-term and long-term memory (ITM and LTM, respectively) for sensitization also lead to sustained MAPK activation in the SNs. Given these results, we next examined the requirement of MAPK activity in (1) SN-MN synaptic facilitation and (2) memory for sensitization in Aplysia, by inhibiting MEK, the upstream kinase that phosphorylates and activates MAPK. In cellular experiments, we show that MAPK activity is required for ITF of tail SN-tail MN synapses, and, in parallel behavioral experiments, we show that ITM requires MAPK activity for its induction but not its expression. In contrast, short-term memory for sensitization does not require MAPK activity. Finally, 5-HT-induced LTF has been shown previously to require MAPK activity. Here we show that LTM for sensitization also requires MAPK activity. These results provide evidence that MAPK plays important roles specifically in long-lasting phases of synaptic plasticity and memory.

Action Potentials↗
PubMed1997

Differential activation of the caudate nucleus in primates performing spatial and nonspatial working memory tasks.

The caudate nucleus is part of an anatomical network subserving functions associated with the dorsolateral prefrontal cortex (DLPFC). The aim of the present study was to investigate whether the metabolic activity in the striatum reflects specific changes in working memory tasks, which are known to be dependent on the DLPFC, and whether these changes reflect the topographic ordering of prefrontal connections within the striatum. Local cerebral glucose utilization (LCGU) rates were assessed in the striatum by the 14C-2-deoxyglucose method in monkeys that performed a spatial (delayed spatial alternation), a nonspatial (delayed object alternation) visual working memory task, or tasks that did not involve working memory, i.e., a visual pattern discrimination or sensorimotor paradigm. The results show a topographic segregation of activation related to spatial and nonspatial working memory, respectively. The delayed spatial alternation task increases LCGU rates bilaterally by 33-43% in the head of the caudate nucleus, where efferents from the dorsolateral prefrontal cortex project most densely. The delayed object alternation task enhances LCGU rates bilaterally by 32-37% in the body of the caudate nucleus, which is innervated by the temporal cortex. The visual pattern discrimination task similarly activated the body of the caudate, but in a smaller region and only in the right hemisphere. These findings provide the first evidence for metabolic activation of the caudate nuclei in working memory, supporting the role of this nucleus as a node in a neural network mediating DLPFC-dependent working memory processes. The double dissociation of activation observed suggests an anatomical and functional segregation of cortico-striatal circuits subserving spatial and nonspatial cognitive operations.

Animals↗
PubMed2006

Lineage and signal strength determine the inhibitory effect of transforming growth factor beta1 (TGF-beta1) on human antigen-specific Th1 and Th2 memory cells.

TGF-beta1 is a pleotrophic cytokine playing an important role in immune regulation. The impact of TGF-beta1 on immune function is determined by the cell type and the microenvironment. CD4+ T cells exemplify this, by responding to TGF-beta1 in heterogeneous ways based on their level of maturation and state of differentiation. TGF-beta1 leads to suppression of proliferation and cytokine production of naive T cells and influences the outcome of T cell differentiation. In mice, the response of memory T cells to TGF-beta1 is determined by the lineage of the cells. TGF-beta1 causes decreased proliferation of Th1 cells but has little effect on the proliferation of Th2 cells. Here we examined the effect of TGF-beta1 on human Th1 and Th2 memory T cells and show that proliferation of Th1 clones are inhibited by TGF-beta1, whereas Th2 cells are not. Furthermore the sensitivity of individual Th1 clones to TGF-beta1 is linked to the level of activation achieved in culture, but these differences cannot be explained by T cell receptor (TCR) affinity alone. Together this demonstrates that the human T cell response to TGF-beta1 is determined by the environment in which an immune response takes place and the previous immune experience of the cells involved.

Animals↗
PubMed1996

Blimp-1 overcomes the block in IgM secretion in lipopolysaccharide/anti-mu F(ab')2-co-stimulated B lymphocytes.

A combination of signals transmitted through the antigen receptor, membrane-bound cell interaction molecules and cytokine receptors induces B cell proliferation and differentiation into immunoglobulin-secreting or memory cells. It has recently been suggested by Turner et al. (Cell 1994. 77: 297) that the complex changes in gene activities accompanying high levels of immunoglobulin secretion are under the common control of a master regulator, Blimp-1 (B lymphocyte-induced maturation protein). We show here that in naive mouse B cells stimulated with lipopolysaccharide (LPS) alone (which leads to high IgM production), Blimp-1 is highly expressed, while cells co-stimulated with LPS and anti-mu F(ab')2 show low levels of Blimp-1 mRNA and no longer secrete Ig. I gamma 1 sterile transcripts are, however, up-regulated after receptor co-ligation. Addition of interleukin (IL)-2 and IL-5 to LPS + anti-mu F(ab')2-treated primary B cells led to up-regulation of Blimp-1 and IgM secretion. Transfection of a Blimp-1 expression vector also induced IgM secretion. The data indicate that Blimp-1 is an important regulator of immunoglobulin secretion by primary B cells, and suggest that its level of expression may determine the differentiation to Ig-secreting plasma cells or entrance and maintenance in the memory pool.

Animals↗
PubMed1991

UCHL1+ (CD45RO+) 'memory' T cells predominate in the CD4+ cellular infiltrate associated with allergen-induced late-phase skin reactions in atopic subjects.

We have previously shown that CD4+ T lymphocytes accumulated at the site of allergen induced late-phase reactions (LPR) in the skin of atopic subjects. In order to determine whether these were predominantly 'memory' or 'naive' cells, monoclonal antibodies recognizing isoforms of the CD45 common leucocyte antigen and immunocytochemical methods were used to study the composition of the T cell infiltrate. Allergen-induced late-phase skin reactions were biopsied 6, 24 or 48 h after allergen challenge. Memory (CD45RO+/UCHL1+) T cells predominated and few naive (CD45RA+/Leu18+) cells were identified. Double immunofluorescence was used to confirm that the UCHL1+ and Leu 18+ cells were CD4+ T lymphocytes. The selective recruitment of memory T cells to LPR sites is consistent with the active involvement of T lymphocytes in atopic allergic inflammation. A possible alternative explanation for apparently selective recruitment is the differential expression of endothelial adhesion molecules on memory and naive T lymphocytes.

Antigens, Differentiation↗
PubMed2006

Dissociable parietal systems for primacy and subsequent memory effects.

The frequently observed superior memory for the first items on a list is referred to as primacy. The aetiology of this effect in terms of cognitive processes and their neural substrate is subject to an ongoing debate. However, the brain areas generally involved in successful encoding are well described by subsequent memory studies in which activity during encoding is correlated with memory performance. We employed an object-location association paradigm to differentiate the neural correlate of the primacy from the subsequent memory effect. Activity in the intraparietal sulcus predicted memory performance across all encoding positions. Increased activity in the inferior parietal lobe and angular gyrus resulted exclusively in a more efficient encoding of the first item presented. These areas are part of the ventral frontoparietal network involved in stimulus driven attention. Our results implicate the relatively elevated attention to the first item probably due to its contextual distinctiveness, as a major contributor to the primacy effect.

Adult↗
PubMed2004

Disturbing visual working memory: electrophysiological evidence for a role of the prefrontal cortex in recovery from interference.

Single cell recordings in monkeys support the notion that the lateral prefrontal cortex (PFC) controls reactivation of visual working memory representations when rehearsal is disrupted. In contrast, recent fMRI findings yielded a double dissociation for PFC and the medial temporal lobe (MTL) in a letter working memory task. PFC was engaged in interference protection during reactivation while MTL was prominently involved in the retrieval of the letter representations. We present event-related potential data (ERP) that support PFC involvement in the top-down control of reactivation during a visual working memory task with endogenously triggered recovery after visual interference. A differentiating view is proposed for the role of PFC in working memory with respect to endogenous/exogenous control and to stimulus type. General implications for binding and retention mechanisms are discussed.

Adult↗
PubMed2005

Enhancement of cellular memory by reducing stochastic transitions.

On induction of cell differentiation, distinct cell phenotypes are encoded by complex genetic networks. These networks can prevent the reversion of established phenotypes even in the presence of significant fluctuations. Here we explore the key parameters that determine the stability of cellular memory by using the yeast galactose-signalling network as a model system. This network contains multiple nested feedback loops. Of the two positive feedback loops, only the loop mediated by the cytoplasmic signal transducer Gal3p is able to generate two stable expression states with a persistent memory of previous galactose consumption states. The parallel loop mediated by the galactose transporter Gal2p only increases the expression difference between the two states. A negative feedback through the inhibitor Gal80p reduces the strength of the core positive feedback. Despite this, a constitutive increase in the Gal80p concentration tunes the system from having destabilized memory to having persistent memory. A model reveals that fluctuations are trapped more efficiently at higher Gal80p concentrations. Indeed, the rate at which single cells randomly switch back and forth between expression states was reduced. These observations provide a quantitative understanding of the stability and reversibility of cellular differentiation states.

Cell Differentiation↗
PubMed2001

Effects of olanzapine and other antipsychotics on cognitive function in chronic schizophrenia: a longitudinal study.

This study aimed to determine the effect of olanzapine and other antipsychotic drugs on cognitive functions after 6months of treatment. Baseline, 3month and 6month psychopathological and cognitive evaluations were made. Thirty-eight partially responsive outpatients with DSM-IV chronic schizophrenia diagnosis were included in the study. On the indication of their attending psychiatrists, 21 patients initiated treatment with olanzapine, and 17 remained on their previous treatment with other antipsychotic drugs. Cognitive assessments were blind to medication and psychopathological status. The olanzapine group presented a significantly greater improvement in negative symptomatology and verbal memory than the comparison group in repeated-measures of MANOVAs between baseline, 3month and 6month assessments. These differences remained statistically significant after covarying out gender, treatment with other atypical antipsychotics, biperidene doses and changes in positive and negative symptoms. In order to match previous differences between groups, cognitive baseline scores for each test were introduced as covariates, resulting in a significant improvement for the olanzapine group in negative symptomatology and the interference task of the Stroop test.We then re-analyzed the data, dividing the comparison group into two groups: risperidone-treated patients (n=9) and patients receiving conventional antipsychotic drugs (n=8). Post-hoc analyses between groups were carried out with baseline cognitive assessment as covariate. The olanzapine group improved significantly more than the risperidone group in negative symptomatology and in the interference task of Stroop test. The improvement in the number of categories of the Wisconsin Card Sorting Test was higher in risperidone patients than in those receiving olanzapine or conventional antipsychotic treatment. Conventional antipsychotic drugs did not present a significant improvement over atypical antipsychotic drugs in any cognitive function. In summary, in patients suffering from chronic schizophrenia, atypical antipsychotic agents were associated with slight differential improvements over time in attentional, verbal memory and executive functions compared with conventional neuroleptic drugs. No differential improvements were found in social functioning, verbal fluency, non-verbal domains of memory or visuo-motor abilities.

Adult↗
PubMed1999

The differential maturation of two processing rates related to digit span.

Recent studies have proposed that rapid-speaking durations predict short-term memory spans. However, N. Cowan et al. (1998, Journal of Experimental Psychology: General, 127, 141-160) found two separate types of processing durations related to digit span for children in Grade 1 (7-8 years), Grade 3 (9-10 years), and Grade 5 (11-12 years): rapid-speaking durations (thought to index the rate of covert articulation) and the durations of interword pauses in the memory span task responses (thought to index the rate of short-term memory retrieval). The present analysis additionally establishes the differential maturation of those two durations. Within-age correlations between span and rapid-speaking durations were significant only in first graders; correlations between span and interword pauses, only in fifth graders. When subsamples were selected to match spans across age groups, both types of duration also were matched between Grades 1 and 3. However, fifth graders had considerably shorter interword pauses than their third-grade counterparts. Thus, a particular memory span is accompanied by different profiles of processing rates in children of different ages.

Age Factors↗
PubMed2006

Altered brain activity processing in high-anxiety rodents revealed by challenge paradigms and functional mapping.

Pathological anxiety involves aberrant processing of emotional information that is hypothesized to reflect perturbations in fear/anxiety pathways. The affected neurobiological substrates in patients with different anxiety disorders are just beginning to be revealed. Important leads for this research can be derived from findings obtained in psychopathologically relevant rodent models of enhanced anxiety, by revealing where in the brain neuronal processing in response to diverse challenges is different to that in animals with lower anxiety levels. Different functional mapping methods in various rodent models, including psychogenetically selected lines or genetically modified animals, have been used for this purpose. These studies show that the divergent anxiety-related behavioral response of high-anxiety- vs. normal and/or low-anxiety rodents to emotional challenges is associated with differential neuronal activation in restricted parts of proposed fear/anxiety circuitries including brain areas thought to be important in stress, emotion and memory. The identification of neuronal populations showing differential activation depends in part on the applied emotional challenge, indicating that specific facets of elicited fear or anxiety preferentially engage particular parts of the fear/anxiety circuitry. Hence, only the use of an array of different challenges will reveal most affected brain areas. A number of the neuronal substrates identified are suggested as candidate mediators of dysfunctional brain activation in pathological anxiety. Indeed, key findings revealed in these rodent models show parallels to observations in human symptom provocation studies comparing anxiety disorder patients with healthy volunteers. Work to investigate exactly which of the changed neuronal activation patterns in high-anxiety rodents has to be modulated by therapeutic drugs to achieve effective anxiolysis and via which neurochemical pathways this can be accomplished is at its early stages but has identified a small number of promising candidates. Extending these approaches should help to provide further insight into these mechanisms, revealing new leads for therapeutic targets and strategies.

Animals↗