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PubMedDate not supplied

[Relationship between memory tests and volumetry and relaxometry of the hippocampus].

INTRODUCTION AND AIMS: Interdisciplinary research made by neuropsychologist, neurologists and radiologists is making possible descriptions of the anatomic bases of memory. The hippocampus is one of the main structures related to memory processing. The aim of the present study was to study the relationship between verbal and visual memory, and the volumetry and relaxometry of the. PATIENTS AND METHODS: 36 patients with temporal lobe epilepsy and mesial temporal sclerosis (MTS). Fist, a neuropsychological assessment of was made the verbal and visual memory. Second, hippocampal structure were studied by magnetic resonance image (hippocampal volumetry and relaxometry). RESULTS AND CONCLUSIONS: Reactive gliosis measured by T2 relaxation time predicted poorer visual memory in patients with right or left MTS. These results indicate that structural damage in right hippocampus implies worse performance in visual memory. Moreover, MTS was found to have negative effects on contralateral memory (poorer verbal memory in right MTS, and poorer visual memory in left MTS). These results could be due to memory compensation. Thus, the memory function associated with the sclerotic hippocampus is adopted by the contralateral structure. Therefore, the more damage there is to the latter, the poorer is the memory functioning.

Epilepsy, Temporal Lobe↗

PubMed1989

Animal studies of brain acetylcholine and memory.

Memory loss is a common feature of aging in the human but not all memories are equally lost. Usually the loss is more severe for the memory of recent events and information rather than the memory of remote events and information. Associated with memory losses of this type is a reduction in levels of cortical acetylcholine and a loss of cholinergic cells of the nucleus basalis magnocellularis. In the rat it is possible to assess two types of memory analogous to recent and remote memories in humans. Reference memory would refer to information concerning the task that is invariant from trial to trial. Working memory would refer to information that changes from trial to trial. In support of the hypothesis that decreases in cholinergic function lead to a differential impairment of working memory, rats trained in this task and given scopolamine showed a specific increase in working memory errors. In more recent studies rats have been trained in a task and then given unilateral neurotoxic lesions of the NBM. These results raise the intriguing possibility that degeneration of the NBM and associated memory impairment seen in aging and in Alzheimer's disease may be related to a change in the ratio of these or related endogenous tryptophan metabolites.

Acetylcholine↗

PubMed2002

Risk to verbal memory following anterior temporal lobectomy in patients with severe left-sided hippocampal sclerosis.

BACKGROUND: Previous investigations indicate low risk for memory loss following anterior temporal lobectomy (ATL) in patients with severe hippocampal sclerosis (HS) compared with patients with mild HS. However, these conclusions have been established primarily with group-level analyses. OBJECTIVE: To investigate individual base rate risk for verbal memory loss following ATL in patients who have pathologically verified mild, moderate, or severe HS. PATIENTS AND METHODS: One hundred fifteen patients with unilateral temporal lobe epilepsy (68 with left-sided and 47 with right-sided epilepsy) were included. Acquisition, retrieval, and recognition components of verbal memory, as measured by the California Verbal Learning Test, were assessed before and after ATL. Postoperatively, the degree of neuronal loss and reactive gliosis of the hippocampus was assessed via a 3-tiered rating system establishing mild, moderate, and severe pathologic features. Patients with preoperative magnetic resonance imaging-based evidence of lesions outside the mesial temporal area (side of surgical resection) were excluded. RESULTS: Neither seizure laterality nor severity of HS was associated with preoperative verbal memory performance. Postoperatively, the left-sided ATL group demonstrated significant decline across the acquisition (P<.01), retrival (P<.001), and recognition (P<.001) verbal memory components compared with the right-sided ATL group. Patients who underwent left-sided ATL and had mild HS displayed the largest magnitude and percentage proportion of postoperative decline across all verbal memory components. However, 28 (48%) of the 58 patients who underwent left-sided ATL and who had moderate and severe HS displayed statistically reliable declines on retrieval aspects of verbal memory. Most patients undergoing right-sided ATL, regardless of the extent of hippocampal pathologic features, displayed no postoperative memory change. CONCLUSIONS: Substantial individual heterogeneity of memory outcome exists across groups of patients undergoing ATL, with various degrees of pathologically verified HS. Patients undergoing left-sided ATL who have mild HS seem at greatest risk for broad-spectrum verbal memory decline. However, when examining outcome on a patient-by-patient basis, many patients undergoing left-sided ATL who have moderate to severe HS were also vulnerable to verbal memory loss. This risk seems selective to a retrieval-based aspect of verbal memory.

Adolescent↗

PubMed1980

Memory B cells at successive stages of differentiation: expression of surface IgD and capacity for self renewal.

In recent studies, we have characterized two memory B cell populations capable of giving rise to IgG antibody-producing cells in adoptive recipients. One population carries surface IgD gives rise to predominantly low-affinity antibody responses; the other lacks detectable surface IgD and gives rise to predominatly high-affinity responses. These memory populations often coexist in individual donors for long periods of time; however, in strongly stimulated donors, the IgD+ population is lost after several weeks, and nearly all detectable B cell memory is IgD- thereafter. In this publication, we show that the IgD+ and IgD- memory populations represent B cells at two successive stages of antigen-dependent differentiation. We used the fluorescence-activated cell sorter (FACS) in a double isolation and transfer protocol to show directly that FACS-isolated IgD+ memory cells transferred to adoptive recipients give rise both to IgG antibody-producing cells and to an expanded memory population that is predominantly IgD-. We also show that FACS-isolated IgD- memory populations from the original donor "self-renew" (i.e. give rise to more IgD- memory) in adoptive recipients and that these events require supplementation of the isolated memory cells with carrier-primed T cells and antigen. In discussing these findings, we integrate our data with previous evidence on the expression of surface IgG on memory B cells to create an updated view of surface Ig expression during memory development. We also consider these findings in the light of our recent suggestion that the loss of IgD receptors facilitates affinity maturation in the more mature (IgD-) memory population.

Animals↗

PubMed1992

Tissue-specific migration pathways by phenotypically distinct subpopulations of memory T cells.

A proportion of T cells recirculate in a tissue-selective manner. Recent studies which showed that the skin-tropic subset of T cells was of memory/activated type, led us to examine whether the preferential homing of T cells to the gut also involved memory T cells, and if so whether these memory T cells were phenotypically distinct from other memory T cells. Lymphocytes migrating through the gut and the skin of sheep was collected by cannulating the lymphatic ducts draining these tissues. Both naive and memory T cells were found to recirculate through the gut, although only memory T cells migrated through the skin. However, when T cells from the gut were labeled with fluorescein isothiocyanate and assessed for their migration back to the gut, it was the memory population which showed a tropism for the gut. Gut-tropic memory T cells migrated poorly through the skin, indicating that these cells were distinct from skin-tropic memory T cells. This was confirmed by phenotypic analysis. Gut memory T cells expressed very low levels of the alpha 6 and beta 1 integrins, in contrast to skin memory T cells which expressed high levels. There was no evidence for heterogeneity within the naive T cell population, which migrated preferentially to lymph nodes. This migration pattern could be explained in part by the high expression of the L-selectin (lymph node homing receptor, LAM-1) on naive T cells, in contrast to memory T cells from gut or skin which were mostly L-selectin negative. These results in sheep indicate that subsets of alpha/beta memory T cells show tissue-selective migration patterns, which probably develop in a particular environment following encounter with antigen.

Animals↗

PubMed2005

Novel phenotypes and migratory properties distinguish memory CD4 T cell subsets in lymphoid and lung tissue.

Memory T cells are heterogeneous in expression of lymph node homing receptors, delineating "central-memory" (TCM, CD62Lhi/CCR7+) and "effector-memory" (TEM, CD62Llo/CCR7-) subsets that migrate to lymphoid and non-lymphoid tissues, respectively. It is not known how these subsets arise or how homing receptor expression and tissue origin determine their functional and migratory properties. Here, we investigated the role of CD62L expression in the generation, function, distribution and migration of heterogeneous memory CD4 T cells specific for influenza hemagglutinin (HA). We found that CD62Lhi and CD62Llo memory subsets are generated independent of CD62L expression by the activated precursor, and both subsets distribute into spleen and lung. Functionally, spleen- and lung-derived CD62L memory subsets produce effector cytokines at similar kinetics but differ strikingly in cell surface phenotype and migration: the CD62Llo memory subset expresses a classic memory phenotype (CD45RBlo/CD44hi/CD11a(hi)), while the CD62Lhi subset expresses an unconventional phenotype (CD45RBhi/CD44int/CD11a(int)), defining a new polyclonal memory subset. The CD62Lhi subset also trafficked more efficiently than CD62Llo cells into lymph nodes; however, only lung but not spleen CD62Llo memory T cells homed to lung. Our results reveal novel phenotypic heterogeneity of memory CD4 T cells co-segregating with CD62L expression and tissue-specific tropism of non-lymphoid memory CD4 T cells.

Animals↗

PubMed2004

No association between subjective memory complaints and apolipoprotein E genotype in cognitively intact elderly.

OBJECTIVE: This cross-sectional study examined the relationship between subjective memory complaints and the apolipoprotein epsilon 4 allele (epsilon4), a genetic risk factor for Alzheimer's disease (AD), among cognitively normal subjects identified from a community memory screening. DESIGN: The sample comprised 232 consecutive white non-Hispanic older adults who presented to a free community-based memory-screening program at a University affiliated memory disorders center. Participants were classified as cognitively normal based on scores on the age and educated adjusted Folstein Mini-Mental Status Exam (MMSAdj) and a brief Delayed Verbal Recall Test (DRT). Subjects were assessed for APOE genotype, subjective memory complaints (Memory Questionnaire, MQ), depressive symptoms (Hamilton Depression Rating Scale, HDRS), and history of four major medical conditions that have been associated with memory loss (stroke/transient ischemic attack [TIA], atherosclerotic heart disease, hypertension, and diabetes). A hierarchical regression analysis was performed to examine the association between APOE genotype and memory complaints after controlling for a host of potential confounding factors. RESULTS: The APOE epsilon4 allele frequency for cognitively normal subjects was 0.13. Subjective memory complaints were predicted by depressive symptoms and a history of stroke/TIA. They were not associated with APOE genotype, MMSAdj score, DRT score, age, education, gender, and reported history of atherosclerotic heart disease, hypertension, or diabetes. CONCLUSION: The results did not suggest an association between subjective memory complaints and the APOE epsilon4 allele in this sample of cognitively intact subjects. This indicates that memory complaints may confer risk for future dementia through pathways independent of APOE genotype. The results also show that older adults with memory complaints are at increased risk for underlying depression.

Aged↗

PubMed2005

Subjective memory complaints in Chinese subjects with mild cognitive impairment and early Alzheimer's disease.

BACKGROUND: Mild cognitive impairment (MCI) represents a transitional state between normal aging and dementia. However, there is inconsistent opinion as to the validity of subjective memory complaints as a criterion for diagnosis. OBJECTIVE: This study aimed to examine the potential significance of applying a short memory questionnaire in the assessment of Chinese subjects with MCI and early dementia. METHODS: Three hundred and six ambulatory Chinese subjects were recruited. Each participant completed a short memory questionnaire. They were also assessed with the Chinese versions of the mini-mental state examination (CMMSE), Alzheimer's disease assessment scale-cognitive subscale (ADAS-Cog), category verbal fluency test (CVFT) and span tests. Severity of cognitive impairment was evaluated using the Clinical Dementia Rating (CDR); subjects with CDR 0.5 were further classified into MCI not demented (MCIND) and MCI possible incipient dementia (MCIID) depending on the subscale scores of CDR. RESULTS: An increasing frequency of memory complaints with increasing CDR was observed (Kruskal Wallis test, chi square = 21.29, df 3, p < 0.001). With a cutoff of 3 or more memory complaints, the memory questionnaire demonstrated a sensitivity of 65.3% and 70.4% in identifying subjects with incipient and early dementia respectively. Significant associations between memory complaints and most cognitive test performance were found (Spearman's correlations, p < 0.01). Logistic regression analysis revealed that educational level, the memory questionnaire, ADAS-Cog total and delayed recall scores were significant predictors of MCIID status. CONCLUSIONS: The findings suggested that a short memory questionnaire is useful in the screening of MCI, particularly in subjects who already present with subtle functioning disturbances. Subjective memory complaints were significant correlated with objective performance of memory functions, reflecting the usefulness of memory complaints in the assessment of MCI.

Aged↗

PubMed2001

Memory rehabilitation in Alzheimer's disease: a review of progress.

BACKGROUND: Memory rehabilitation is a sadly misrepresented area of applied research in Alzheimer's disease. OBJECTIVES: To gather and evaluate recent evidence for the clinical effectiveness or ecologically validity of memory rehabilitation for mild to moderate Alzheimer's patients. METHODS: Computerised searches and some handsearching were conducted spanning the last five years, from 1995 to 2000, inclusively. Criteria for inclusion in this overview involved the use of a precise memory rehabilitation technique within an experimental study design applied to Alzheimer's patients with pre- and post-treatment evaluation. FINDINGS: Three potential levels of memory rehabilitation procedures with proven clinical or pragmatic efficacy were identified. The first level bears on the facilitation of residual explicit memory with structured support both at encoding and at subsequent recall; the second level of memory rehabilitation exploits the relatively intact implicit memory system (priming and procedural memory); the last deals with finding ways of coping with the patient's limited explicit memory capacities through the use of external memory aids. A proposal of suggestions for good practice and future research in memory rehabilitation is also offered with the hope to spur further development in this rapidly expanding area of applied research. CONCLUSION: The available evidence shows that alternative and innovative ways of memory rehabilitation for Alzheimer's patients can indeed be clinically effective or pragmatically useful with a great potential for use within the new culture of a more graded and proactive type of Alzheimer's disease care.

Adaptation, Psychological↗

PubMed2005

Hippocampus and remote spatial memory in rats.

Damage to the hippocampus typically produces temporally graded retrograde amnesia, whereby memories acquired recently are impaired more than memories acquired remotely. This phenomenon has been demonstrated repeatedly in a variety of species and tasks. It has also figured prominently in theoretical treatments of memory and hippocampal function. Yet temporally graded retrograde amnesia has not been demonstrated following hippocampal damage in spatial tasks like the water maze. We have assessed recent and remote spatial memory following hippocampal lesions in three different tests of spatial memory: (1) the standard water maze; (2) the Oasis maze, a dry-land version of the water maze; and (3) the annular water maze, where training and testing occur within a circular corridor. Training protocols were developed for each task such that retention of spatial memory could be expressed after very long retention intervals. In addition, retention in each task was assessed with single probe trials so that the assessment of remote memory did not depend on the ability to relearn across multiple trials. The findings were consistent across the three tasks. In the standard water maze (Experiment 1), spatial memory was impaired after training-surgery intervals of 1 day, 8 weeks, or 14 weeks. Similarly, in the Oasis maze (Experiment 2), spatial memory was impaired after training-surgery intervals of 1 day and 9 weeks. Finally, in the annular water maze (Experiment 3), spatial memory was impaired after training-surgery intervals of 9 weeks and 14 weeks. Dorsal hippocampal lesions impaired performance to the same extent as complete lesions. The impairment in remote spatial memory could reflect disruption of previously acquired spatial information. Alternatively, it is possible that in these tasks hippocampal lesions might produce an impairment in performance that prevents the expression of an otherwise intact spatial memory.

Amnesia, Retrograde↗

PubMedDate not supplied

Behavioral methods for measuring effects of drugs on learning and memory in animals.

This review describes methods for measuring effects of drugs on learning and memory in animals, proceeding from relatively simple nonassociative learning (habituation) to classical and instrumental conditioning, and concluding with complex measures for measuring learning and memory repeatedly in the individual animal. Procedures for separating drug effects specific to learning and memory from non-specific effects on activity, motivation, sensory and motor capacity, etc., were emphasized. For each method, selected experimental examples were presented which described the action of drugs on learning and memory, elucidated the behavioral processes involved in the drug effects, or illustrated methodological points. The various procedures used to measure drug effects on learning and memory in animals have yielded a bewildering array of often-contradictory results. Quantitative differences in effectiveness of drugs in the different procedures are common. Drugs (for example, the nootropics) that alter learning or memory in a few procedures may be totally without activity in many others. How are these discrepancies to be interpreted? The apparent inconsistencies in the data can, for the most part, be understood in terms of the nature of learning and memory. "Learning" and "memory" are hypothetical processes presumed to underlie enduring changes in behavior resulting from the organism's interaction with environmental stimuli. Given such a broad definition, the prevalence of inconsistencies in the data is hardly surprising. It is unlikely that the same mechanisms should underlie all of the wide variety of behavioral changes included under the rubrics "learning" or "memory." (For a contrary view, based on consistencies among results obtained in the diverse procedures, see Zornetzer). How, then, should drug effects on learning and memory be identified or measured? The first step, of course, is to rule out those drug effects that do not conform to the definition of learning or memory. This review has described strategies and procedures by which this can be accomplished. However, even when this is done there is no single procedure that can detect drug effects on learning and memory in general, nor, in view of the heterogeneous behaviors involved, is it likely that such a universal procedure will ever be found. Thus, a multi-faceted strategy will be required. Some of the simpler procedures described in this review may be adequate for the initial identification of interesting effects.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1997

Working memory: a view from neuroimaging.

We have used neuroimaging techniques, mainly positron emission tomography (PET), to study cognitively driven issues about working memory. Two kinds of experiments are described. In the first kind, we employ standard subtraction logic to uncover the basic components of working memory. These studies indicate that: (a) there are different working-memory systems for spatial, object, and verbal information (with the spatial system localized more in the right hemisphere, and the verbal system more in the left hemisphere); (b) within at least the spatial and verbal systems, separable components seem to be responsible for the passive storage of information and the active maintenance of information (with the storage component being localized more in the back of the brain, and the maintenance component in the front); and (c) there may be separate components responsible for processing the contents of working memory (localized in prefrontal cortex). In our second kind of experiment we have focused on verbal working memory and incrementally varied one task parameter-memory load-in an effort to obtain a more fine-grained analysis of the system's operations. The results indicate that all relevant components of the system show some increase in activity with increasing memory load (e.g., the frontal regions responsible for verbal rehearsal show incremental increases in activation with increasing memory load). In contrast, brain regions that are not part of the working-memory system show no effect of memory load. Furthermore, the time courses of activation may differ for regions that are sensitive to load versus those that are not. Taken together, our results provide support for certain cognitive models of working memory (e.g., Baddeley, 1992) and also suggest some distinctions that these models have not emphasized. And more fundamentally, the results provide a neural base for cognitive models of working memory.

Brain↗

PubMed1998

Posttraining estrogen and memory modulation.

The present paper provides a review of recent research carried out in this laboratory investigating the effects of posttraining peripheral and intrahippocampal injection of estradiol on memory in rats, and estradiol-acetylcholine interactions in memory modulation. Ovariectomized rats received an eight-trial training session in a hippocampal-dependent hidden platform water maze task. Immediately following training, rats received a posttraining peripheral or intrahippocampal injection of estradiol-cyclodextrin complex or vehicle. Twenty-four hours later rats were returned to the maze for a retention test session, and latency to escape was used as a measure of memory for the previous day's training. Peripheral posttraining injection of estradiol enhances memory relative to vehicle-treated rats. Injections of estradiol given 2 h posttraining has no effect on retention, indicating a time-dependent effect of estradiol on memory storage processes. A time-dependent memory enhancing effect of posttraining intrahippocampal injections of estradiol has also been observed in both male and ovariectomized female rats. The memory enhancing effect of peripheral posttraining injection of estradiol in ovariectomized rats is blocked by a subeffective dose of the acetylcholine muscarinic receptor antagonist scopolamine, suggesting that estradiol interacts with cholinergic systems in memory modulation. Concurrent peripheral posttraining injection of a subeffective dose of estradiol and a subeffective dose of the cholinergic agonist oxotremorine produces a synergistic memory enhancing effect. The findings suggest that: (1) estradiol selectively influences memory storage independent of an effect on nonmnemonic processes, (2) the hippocampus is a potential neuroanatomical site of action mediating estrogenic effects on memory, and (3) estradiol interacts with cholinergic systems in memory modulation.

Animals↗

PubMed1998

Human prefrontal cortex is not specific for working memory: a functional MRI study.

Lesion studies in monkeys have provided evidence that lateral prefrontal cortex is necessary for working memory, the cognitive processes involved in the temporary maintenance and manipulation of information. Monkey electrophysiological studies, however, have also observed prefrontal neuronal activity associated with cognitive processes that are nonmnemonic. We tested the hypothesis that the same regions of human prefrontal cortex that demonstrate activity during working memory tasks would also demonstrate activity during tasks without working memory demands. During echoplanar fMRI imaging, subjects performed a three-condition experiment (working memory task, nonworking memory task, rest). In the working memory task, subjects observed serially presented stimuli and determined if each stimulus was the same as that presented two stimuli back. The nonworking memory task in Experiment 1 required subjects to identify a single predetermined stimulus; in Experiment 2, subjects were required to make a button press to every stimulus. In all subjects in both experiments, the working memory task exhibited greater prefrontal cortical activity compared to either nonworking memory task. In these same prefrontal regions, greater activation was also observed during both nonworking memory tasks compared to rest. We conclude that human lateral prefrontal cortex supports processes in addition to working memory. Thus, reverse inference of the form "if prefrontal cortex is active, working memory is engaged" is not supported.

Adult↗

PubMed1998

Individual differences in spatial memory and striatal ChAT activity among young and aged rats.

Individual differences in spatial memory among young and aged rats were assessed using memory tasks related to integrity of the hippocampus and the neostriatum. Relationships were then examined between measures of spatial memory and regional choline acetyltransferase (ChAT) activity, a marker for cholinergic integrity. Twenty-four-month-old Long-Evans rats were impaired in comparisons with 6-month-old rats on measures of place learning, working memory, reference memory, and perseveration in water-maze tasks. Aged rats that were impaired on one measure of memory, however, were not necessarily impaired on other measures. ChAT activity in the ventromedial and dorsolateral neostriatum of aged rats was significantly reduced in comparisons with young rats whereas no difference was found in the hippocampus. Aged rats with the most ChAT activity in the anterior ventromedial neostriatum performed best on the place-learning and reference memory tasks but also made the most perseverative errors on the working memory task. In addition, young and aged rats with the most ChAT activity in the anterior dorsolateral neostriatum were those with the least accurate working memory. No relationships were found between ChAT activity in the hippocampus and spatial memory. Thus age-related memory impairment has components that can be segregated by measuring relationships between cholinergic integrity in subregions of the anterior neostriatum and memory tasks with different strategic requirements.

Aging↗

PubMed2002

Effects of stress hormones on traumatic memory formation and the development of posttraumatic stress disorder in critically ill patients.

A majority of patients after intensive care treatment report traumatic memories from their stay in the intensive care unit (ICU). Traumatic memories can be associated with the development of posttraumatic stress disorder (PTSD) in a subpopulation of these patients. In contrast to other patient populations at risk for PTSD, patients in the ICU often receive exogenously administered stress hormones like epinephrine, norepinephrine, or cortisol for medical reasons and are extensively monitored. ICU patients therefore represent a suitable population for studying the relationship between stress hormones, traumatic memories, and the development of PTSD. Studies in long-term survivors of ICU treatment demonstrated a clear and vivid recall of different categories of traumatic memory such as nightmares, anxiety, respiratory distress, or pain with little or no recall of factual events. The number of categories of traumatic memory recalled increased with the total administered dosages of stress hormones (both catecholamines and cortisol), and the evaluation of these categories at different time points after discharge from the ICU showed better memory consolidation with higher dosages of stress hormones administered. However, the administration of stress doses of cortisol to critically ill patients resulted in more complex findings as it caused a significant reduction in PTSD symptoms measured after recovery. This effect can possibly be explained by a differential influence of cortisol on memory. Increased serum cortisol levels not only result in consolidation of emotional memory but are also known to cause a temporary impairment in memory retrieval which appears to be independent of glucocorticoid effects on memory formation. Disrupting retrieval mechanisms with glucocorticoids during critical illness may therefore act protectively against the development of PTSD by preventing recall of traumatic memories. Our findings indicate that stress hormones influence the development of PTSD through complex and simultaneous interactions on memory formation and retrieval. Our studies also demonstrate that animal models of aversive learning are useful in analyzing and predicting clinical findings in critically ill humans.

Affect↗

PubMed2002

Migration of primary and memory CD8 T cells.

Our results indicate that a substantial proportion of the antimicrobial CD8 and CD4 T cell response is focused in non-lymphoid tissues. This finding makes teleological sense since maximum protection against infection is better served by the widespread presence of effector and memory cells. In the case of CD8 T cells, it appears that irrespective of the site at which initial activation of naive cells occurs, the end result is production of effector cells with broad migratory capabilities. Memory T cells perhaps have more restricted migratory abilities as compared to effector cells, although this needs to be tested definitively. Our results suggest that memory CD8 T cells in the intestinal LP may not be part of the recirculating pool of memory cells, though our data does not preclude the possibility that migrants from outside the mucosa contribute to the LP memory pool. Our data also demonstrates that CD8 memory T cells in non-lymphoid tissue exhibit heightened effector function as compared to their splenic counterparts. Whether these findings indicate the existence of distinct lineages of memory cells remains to be seen. The functional abilities of migrating memory cells could be modulated by the migration process and/or by the environmental milieu of a particular tissue. Although the development of CD8 memory T cells is a complex process requiring multiple signalling pathways, we identified IL-7 as an important player in memory generation. Much further work is needed to decipher the cellular and molecular mechanisms of memory induction as well as to learn the in vivo functional significance of memory cell subsets.

Animals↗

PubMed2005

Combined D1/D2 receptor stimulation under conditions of dopamine depletion impairs spatial working memory performance in humans.

RATIONALE: The mesocortical dopamine system is regarded as an important modulator of working memory. While it has been established that stimulation of the D1/D2 receptor in primates can improve spatial working memory performance, findings in humans are less consistent. Recent studies in humans suggest that global depletion of dopamine via tyrosine/phenylalanine depletion may impair spatial working memory performance, although these results are also inconsistent, and it has been suggested that task differences may partly underlie the inconsistent findings. OBJECTIVES: This study had two aims: (1) to investigate the effects of acute tyrosine depletion (TPD) on a number of working memory tasks and (2) to examine whether stimulation of D1/D2 receptors under conditions of TPD can attenuate or "reverse" TPD-induced working memory impairments. METHODS: Eighteen healthy male participants performed a spatial working memory delayed-recognition task, non-spatial working memory task and spatial n-back task on three separate occasions, after TPD, TPD and pergolide (D1/D2 agonist), and placebo. RESULTS: TPD did not impair working memory performance on any of the tasks administered. However, stimulation of D1/D2 receptors under TPD conditions caused a subtle impairment in spatial working memory performance. CONCLUSIONS: The finding that D1/D2 stimulation under TPD conditions impairs working memory highlights the complexity of functional effects of augmenting dopaminergic transmission within a dopamine-depleted state. The lack of TPD-related effects on a range of working memory tasks questions the reliability of TPD as a modulator of dopamine function and working memory performance in humans.

Adolescent↗