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Results for “memory differentiation”

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At least 649 records · Page 36Linked to original sources
PubMed1991

Differential effects of unilateral temporal lobectomy on visuospatial memory and attention.

We investigated free recall of visuospatial arrays in a free-field format in epileptic patients following unilateral temporal lobectomy (TL) (left = 15, right = 17). TL patients exhibited leftward deviation in right hemispace, but more variable response in left hemispace, a pattern that has been observed in healthy adults. This finding is postulated to result from combined preferential right cerebral activation and a tendency to err toward peri-personal space. Temporal lobectomy affected overall leftward deviation by initially shifting deviation more toward the side of lesion. The initial directional shift in immediate memory dissipated over time suggesting that these subtle attentional shifts may be compensated by learning. Consistent with differential cerebral hemispheric mechanisms, absolute vertical errors were greater in right than left TL patients, and absolute horizontal errors were worse in right hemispace.

Adult↗
PubMed2004

Signaling control of memory T cell generation and function.

Memory T cells exhibit low activation thresholds and mediate rapid effector responses when recalled by antigen; contrasting the higher activation threshold, slower responses and predominant IL-2 production by naive T cells. While the sequence of intracellular events coupling the T cell-receptor (TCR) to naive T cell activation is well characterized, biochemical control of memory T cell differentiation and function remains undefined. In this review, we will discuss recent developments in T cell-receptor signal transduction as they pertain to memory T cells, and will discuss how signal dampening may drive memory generation, and more efficient spatial organization of signaling molecules may promote rapid recall responses.

Animals↗
PubMed2005

The effects of clozapine and risperidone on spatial working memory in schizophrenia.

OBJECTIVE: The purpose of this investigation was to evaluate the effects of clozapine and risperidone on spatial working memory in patients with schizophrenia. METHOD: Spatial working memory performance was evaluated at baseline and after 17 and 29 weeks in 97 patients with schizophrenia participating in a multisite trial. RESULTS: Compared with baseline performance while receiving conventional antipsychotic medication, risperidone improved, and clozapine worsened, spatial working memory performance. CONCLUSIONS: The differential effects of these medications on spatial working memory may be due to the anticholinergic effects of clozapine and prefrontal dopamine-enhancing effects of risperidone.

Adult↗
PubMed2005

Central memory and effector memory subsets of human CD4(+) and CD8(+) T cells display differential sensitivity to TNF-{alpha}-induced apoptosis.

Upon activation by antigen, naive T cell subsets undergo proliferation and differentiation into effector cells, followed by the generation of a pool of memory T cells. Based upon migration pattern and functions, they are classified into central memory (predominantly homing to the lymph nodes) and effector memory (predominantly homing to extralymphoid sites) subsets. These subsets are defined phenotypically by a set of cell surface molecules. In this investigation, we demonstrate that naive and central memory CD4(+) and CD8(+) T cells in humans undergo tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis, whereas effector memory CD4(+) and CD8(+) T cells are relatively resistant to TNF-alpha-induced apoptosis. We also provide evidence for the molecular mechanisms underlying the differential sensitivity of naive and different sets of memory T cells to TNF-alpha-induced apoptosis.

Adolescent↗
PubMed2005

Expression of the immunoregulatory molecule FcRH4 defines a distinctive tissue-based population of memory B cells.

The FcRH4 transmembrane molecule, a member of the Fc receptor homologue family, can potently inhibit B cell receptor (BCR) signaling. We show that cell surface expression of this immunoregulatory molecule is restricted to a subpopulation of memory B cells, most of which lack the classical CD27 marker for memory B cells in humans. The FcRH4+ and FcRH4- memory B cells have undergone comparable levels of immunoglobulin isotype switching and somatic hypermutation, while neither subpopulation expresses the transcription factors involved in plasma cell differentiation. The FcRH4+ memory cells are morphologically distinctive large lymphocytes that express the CD69, CD80, and CD86 cell activation markers. They are also shown to be poised to secrete high levels of immunoglobulins in response to stimulation with T cell cytokines, but they fail to proliferate in response either to BCR ligation or Staphylococcus aureus stimulation. A heightened expression of the CCR1 and CCR5 chemokine receptors may facilitate their preferential localization in lymphoid tissues near epithelial surfaces. Cell surface FcRH4 expression thus marks a unique population of memory B cells with distinctive morphology, functional capabilities, and tissue localization.

Antibodies, Monoclonal↗
PubMedDate not supplied

Priming of CD4+ T cells and development of CD4+ T cell memory; lessons for malaria.

CD4 T cells play a central role in the immune response to malaria. They are required to help B cells produce the antibody that is essential for parasite clearance. They also produce cytokines that amplify the phagocytic and parasitocidal response of the innate immune system, as well as dampening this response later on to limit immunopathology. Therefore, understanding the mechanisms by which T helper cells are activated and the requirements for development of specific, and effective, T cell memory and immunity is essential in the quest for a malaria vaccine. In this paper on the CD4 session of the Immunology of Malaria Infections meeting, we summarize discussions of CD4 cell priming and memory in malaria and in vaccination and outline critical future lines of investigation. B. Stockinger and M.K. Jenkins proposed cutting edge experimental systems to study basic T cell biology in malaria. Critical parameters in T cell activation include the cell types involved, the route of infection and the timing and location and cell types involved in antigen presentation. A new generation of vaccines that induce CD4 T cell activation and memory are being developed with new adjuvants. Studies of T cell memory focus on differentiation and factors involved in maintenance of antigen specific T cells and control of the size of that population. To improve detection of T cell memory in the field, efforts will have to be made to distinguish antigen-specific responses from cytokine driven responses.

Animals↗
PubMed1989

Evidence for task-dependent memory dysfunction in the aged monkey.

Experimentally naive adult (9-11 years old) and aged (approximately 22-26 years old) female rhesus monkeys were evaluated on 3 neuropsychological tests of memory function. Aged monkeys were impaired in a delayed response test of visuospatial memory when the retention interval of the task was increased from 0 to 10 sec. These animals performed as well as younger subjects, however, at very short delays (0 and 1 sec), when the memory demands of the task were minimal. The same subjects were then trained in a delayed nonmatching to sample (DNMS) test of visual object recognition memory. Although they required significantly more training than the younger subjects to learn the nonmatching principle of the task, aged animals were only minimally impaired when recognition memory was tested at retention intervals ranging from 10 sec to 22 hr. In contrast to their relatively intact performance on the object recognition task, aged monkeys were dramatically impaired in a second version of DNMS that required subjects to remember the temporal order in which objects were presented. These findings support the view that certain memory functions are differentially susceptible to age-dependent deterioration. Since neuropsychological studies in young subjects demonstrate that different brain regions make relatively specific contributions to learning and memory, the task-dependent deficits observed in the aged monkey are important for determining which neural structures mediate age-dependent cognitive dysfunction. According to this perspective, aged monkeys were impaired on tasks known to be sensitive to prefrontal cortical damage, but the same animals performed well on a DNMS procedure that subjects with medial temporal lobe damage fail. These results suggest that prefrontal cortical dysfunction may mediate prominent aspects of age-dependent cognitive impairment in the monkey.

Aging↗
PubMed2005

Recall discriminability: utility of a new CVLT-II measure in the differential diagnosis of dementia.

Memory tests that are in a recall format have almost universally measured accuracy in terms of the number of target items reported by the examinee. However, this traditional scoring method can, in certain cases, result in artificially inflated memory accuracy scores. That is, just as a "yes" response bias and high false-positive rate on recognition testing can artificially inflate a patient's hit rate, so, too, a liberal response bias and high intrusion rate on recall testing can artificially inflate a patient's level of target recall. Recognition tests correct for this problem by using a discriminability measure that provides a single score of hit rate relative to false-positive rate; however, recall tests rarely provide a single score of recall accuracy that corrects for intrusion rate. In the present study, we examined the utility of a new recall discriminability measure that analyzes target recall relative to intrusion rate. Patients with Alzheimer's disease (AD) or Huntington's disease (HD) were administered the CVLT-II, which provides both the traditional measure of target recall and a new measure of recall discriminability. The results indicate that the new recall discriminability measure was superior to the traditional level of target recall measure in distinguishing the recall performance of AD and HD patients. Implications of these results for clinical practice and theories of memory disorder in dementia are discussed.

Adult↗
PubMed1997

Differential T cell receptor-mediated signaling in naive and memory CD4 T cells.

Naive and memory CD4 T cells differ in cell surface phenotype, function, activation requirements, and modes of regulation. To investigate the molecular bases for the dichotomies between naive and memory CD4 T cells and to understand how the T cell receptor (TCR) directs diverse functional outcomes, we investigated proximal signaling events triggered through the TCR/CD3 complex in naive and memory CD4 T cell subsets isolated on the basis of CD45 isoform expression. Naive CD4 T cells signal through TCR/CD3 similar to unseparated CD4 T cells, producing multiple tyrosine-phosphorylated protein species overall and phosphorylating the T cell-specific ZAP-70 tyrosine kinase which is recruited to the CD3zeta subunit of the TCR. Memory CD4 T cells, however, exhibit a unique pattern of signaling through TCR/CD3. Following stimulation through TCR/CD3, memory CD4 T cells produce fewer species of tyrosine-phosphorylated substrates and fail to phosphorylate ZAP-70, yet unphosphorylated ZAP-70 can associate with the TCR/CD3 complex. Moreover, a 26/28-kDa phosphorylated doublet is associated with CD3zeta in resting and activated memory but not in naive CD4 T cells. Despite these differences in the phosphorylation of ZAP-70 and CD3-associated proteins, the ZAP-70-related kinase, p72syk, exhibits similar phosphorylation in naive and memory T cell subsets, suggesting that this kinase could function in place of ZAP-70 in memory CD4 T cells. These results indicate that proximal signals are differentially coupled to the TCR in naive versus memory CD4 T cells, potentially leading to distinct downstream signaling events and ultimately to the diverse functions elicited by these two CD4 T cell subsets.

Amino Acid Sequence↗
PubMed1997

Long-term memory modulation by posttraining epinephrine in rats: differential effects depending on the basic learning capacity.

Effects of posttraining epinephrine on retention of a massed (1 session, 30 trials) 2-way active avoidance task were studied in rats. Immediately after the training session rats received an injection of 0.05 or 0.01 mg/kg ip epinephrine, or distilled water. Retention was tested 11, 20, or 45 days after training, in independent groups of rats. The 20- and 45-day retention was improved in poor-learning rats and disrupted in good-learning rats. It was concluded that the effect (facilitatory or disruptive) of posttraining epinephrine on memory consolidation depends on the basic learning capacity of rats for this task and needs a long time to be expressed.

Animals↗
PubMed2001

A cognitive neuroscience account of posttraumatic stress disorder and its treatment.

Recent research in the areas of animal conditioning, the neural systems underlying emotion and memory, and the effect of fear on these systems is reviewed. This evidence points to an important distinction between hippocampally-dependent and non-hippocampally-dependent forms of memory that are differentially affected by extreme stress. The cognitive science perspective is related to a recent model of posttraumatic stress disorder, dual representation theory, that also posits separate memory systems underlying vivid reexperiencing versus ordinary autobiographical memories of trauma. This view is compared with other accounts in the literature of traumatic memory processes in PTSD, and the contrasting implications for therapy are discussed.

Animals↗
PubMed1982

Comparative aspects of studies of amnesia.

In recent years important advances have been made in reconciling some of the conflicting evidence regarding the contribution of the medial temporal lobe--hippocampal structures to long-term memory in man compared with laboratory animals. Despite the severe amnesic state that is seen clinically in patients, it has nevertheless emerged that both in animals and man damage to the structures leaves learning and retention of certain types of long-term memory tasks intact. The evidence from man suggests that in the amnesic syndrome the integrity is preserved of those forms of long-term memory that do not depend on the operation of a 'mediational' memory system. In particular, items stored in semantic memory can be facilitated by repetition, and simple associations can be formed if no mediating links are required, but impairments are seen in tasks in which memory depends upon the stored benefits of matching, reordering and comparing. A similar characterization seems possible for the results of animal studies. One interpretation of the differential sensitivity of memory tasks in the amnesic syndrome is in terms of a disconnection syndrome which a semantic memory system is detached from a mediational system. The disconnection is postulated to be caused by interruption of those temporal-frontal pathways in which pathology has been found in the brains of amnesic patients, namely the mammillary bodies and the subependymal zone of the thalamus.

Amnesia↗
PubMed2004

Discrete event modeling of CD4+ memory T cell generation.

Studies of memory T cell differentiation are hampered by a lack of quantitative models to test hypotheses in silico before in vivo experimentation. We created a stochastic computer model of CD4+ memory T cell generation that can simulate and track 10(1)-10(8) individual lymphocytes over time. Parameters for the model were derived from experimental data using naive human CD4+ T cells stimulated in vitro. Using discrete event computer simulation, we identified two key variables that heavily influence effector burst size and the persistent memory pool size: the cell cycle dependent probability of apoptosis, and the postactivation mitosis at which memory T cells emerge. Multiple simulations were performed and varying critical parameters permitted estimates of how sensitive the model was to changes in all of the model parameters. We then compared two hypotheses of CD4+ memory T cell generation: maturation from activated naive to effector to memory cells (model I) vs direct progression from activated naive to memory cells (model II). We find that direct progression of naive to memory T cells does not explain published measurements of the memory cell mass unless postactivation expansion of the memory cell cohort occurs. We conclude that current models suggesting direct progression of activated naive cells to the persistent memory phenotype (model II) do not account for the experimentally measured size of the postactivation CD4+, Ag-specific, memory T cell cohort.

Apoptosis↗
PubMed2005

Temporal gradients for media-mediated memory: Italian norms.

Temporal gradient (TG), i.e., differential recall of recent and old memories, is a well known feature of amnesia. A recent study provided evidence of a classical TG for media-mediated events in elderly healthy people, showing that they recall remote events significantly better than recent ones, while a reverse TG, i.e., better recall of more recent events, was demonstrated in younger normal subjects. In the present study we present normative data which, using the same test, allow evaluation of TG in single cases and their qualification as classical or reverse. The normative procedure was also applied to a small sample of subjects with probable Alzheimer's disease or mild cognitive impairment. Norms for TG may be helpful not only to assess healthy people's performance, but also to judge any apparent TG in pathological subjects.

Aged↗
PubMed1989

Differential influences of corticotropin-releasing factor on memory retention of aversive learning and appetitive learning in rats.

The effects of intraamygdala injections of corticotropin-releasing factor (CRF) on memory retention of aversive and appetitive learnings were examined in the present study. Other than confirming the results of a previous study that a moderate dose of CRF (0.1 microgram) injected into the amygdala facilitated retention performance of an inhibitory avoidance task (electric shock punishment) 24 h after training, we have further found that this effect lasted for a week. However, CRF produced a differential dose-response effect upon memory of an appetitive learning paradigm (sexual reinforcement). CRF at 0.01 microgram enhanced retention at both 24-h and 1-week intervals, while CRF at 0.1 microgram impaired retention in the same task at 1 week only. These results confirm that the amygdala is important in memory processing and suggest that the mechanisms involved in the action of CRF on memory retention of aversive and appetitive learnings are different. The possible differences are also discussed.

Amygdala↗
PubMed1994

The role of visual imagery in the retention of information from sentences.

We conducted two experiments to evaluate a multiple-code model for sentence memory that posits both propositional and visual representational systems. Both sentences involved recognition memory. The results of Experiment 1 indicated that subjects' recognition memory for concrete sentences was superior to their recognition memory for abstract sentences. Instructions to use visual imagery to enhance recognition performance yielded no effects. Experiment 2 tested the prediction that interference by a visual task would differentially affect recognition memory for concrete sentences. Results showed the interference task to have had a detrimental effect on recognition memory for both concrete and abstract sentences. Overall, the evidence provided partial support for both a multiple-code model and a semantic integration model of sentence memory.

Adult↗
PubMed1990

Memory, synaptic plasticity and neurotoxins.

Most neurotoxins induce serious impairments in cognitive or intellectual functioning; therefore, the ability of the individual to learn and remember forms a critical component of neurotoxin assessment. In depth investigations of neurotoxin-induced cognitive deficits have assisted in pinpointing the neural site of toxin activity. However, specific impairments in learning and memory can depend on the developmental stage at which the individual is exposed to the toxin, and certain neurotoxins show cognitive lifespan selectivity. There appears to be a basic sequence of events underlying neural development and information storage, and neurotoxins may disrupt this neuronal sequel critical for the storage or expression of "ancestral" or "environmental" memories. Certain primary rules govern the orderly development of the nervous system; these rules or mechanisms allow the expression of "ancestral memories" concerning neuronal differentiation and primitive behaviors. Following birth, these same mechanisms have been retained in a less robust form to allow learning and information storage, or the retention of "environmental memories." Neurotoxins which disrupt learning and memory capacities appear to interfere in this basic sequence of events, with the specific outcome depending on when during lifespan development the neurotoxin intervenes.

Animals↗
PubMed1989

Failure to find residual memory deficits in monkeys after repeated HPNS.

Squirrel monkeys (n = 8) were equated on learning and memory tasks before sustaining 3 separate dives in a laboratory compression chamber. Associative memory was carefully monitored 1 wk before and 3 wk immediately after each dive. The first dive was a shallow, subseizure control dive and the subsequent 2 dives were deep, seizure-inducing dives. Half of the animals were always compressed in He-O2 and half in He-N2-O2 gas, which is known to increase the depth at which tremors and seizures occur. After the control dive there was a slight (10% average) decline in memory performance, but the decline was temporary and recovery was complete by the second postdive week. There was no evidence of residual memory impairments after either of the 2 subsequent seizure-inducing dives. Although addition of nitrogen to the breathing gas significantly elevated thresholds for tremors, it had no differential effect on memory scores. These results are in agreement with studies of human divers that show either no residual impairments or transient, fully recoverable cognitive symptoms after diving.

Animals↗