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PubMed1976

Two stages of B-cell memory development with different T-cell requirements.

We present evidence here for two stages in B-memory cell development, the first of which is T independent and the second T dependent. For these studies, we use a new type of T-deficient mouse (allotype suppressed) which specifically lacks T-helper activity (Th) for a subset of memory B cells responsible for approximately 10% of the overall IgG antibody response. We have shown elsewhere that these mice (SJL X BALB/c hybrids suppressed for Ig-1b) lack Th capable of helping Ig-1b memory cells, although they have normal Th activity for all other IgG memory B cells. This selective Th deficiency allows study of the effects of T depletion on memory development and avidity maturation of one population of B cells under conditions where the bulk of the immune response in the animal is proceeding normally, thus obviating environmental problems due to secondary effects of T depletion. With this sytem, we show that after a single priming dose of 2,4-dinitrophenyl-keyhole limpet hemocyanin, the memory B-cell pool in suppressed and nonsuppressed donors is indistinguishable with respect to magnitude and avidity of the response for all IgG antibodies produced, including Ig-1b antibody, despite the fact that expression of Ig-1b memory cells is prevented in intact Ig-1b-suppressed mice by the absence of Th capbale of cooperating with these memory cells. We have shown elsewhere that virtually all of the Ig-1b memory is carried by Ig-1b bearing cells. In contrast with the lack of suppressor T-cell effect on initial Ig-1b memory cell development, our data show that continued Ig-1b memory development is selectively impaired in suppressed mice. When primed mice are boosted repeatedly with the priming antigen, the average avidity of most of the IgG memory cells increases over 100-fold while there is no avidity increase in the Ig-1b component. To explain these data, we suggest that the development of high avidity memory occurs in two stages. The first stage, which occurs as a result of primary antigenic exposure, is the creation of a pool of IgG-bearing memory cells with a relatively low average avidity for the antigen. The appearance of these first stage memory cells does not require help from (post-thymic) Th, although Th are required for the expression of these memory cells (antibody production). The second stage of B-memory development requires both further antigenic stimulation and B-memory cell interaction with competent Th. This is a continuing process in which the number of memory cells in the pool remains relatively constant but the average avidity of these cells increases with continued antigenic exposure.

Animals↗
PubMedDate not supplied

[Memory disorders in schizophrenia].

The current interest in memory disorders in schizophrenia results from the way perceptions of schizophrenia--whose organic origin is becoming increasingly evident--and memory--according to which there exist not one, but several memories--have developed. Memory disorders in the schizophrenic cannot be considered in isolation from knowledge accumulated in other areas of the cognitive and neuro-sciences; a more detailed understanding of these disorders requires a comparison of the different cognitive approaches, both with each other and with the neurobiological and clinical approaches, so that they can be integrated. Despite numerous methodological and conceptual difficulties, it now appears to have been established that the schizophrenic's memory deficit should be seen in the context of a wider cognitive deficit, that the memory tasks are not all disturbed and that the memory deficit cannot be identified with one specific form of memory. Thus, iconic formation, short-term memory in the traditionally accepted sense and implicit memory are hardly, if at all, affected; in contrast, the early processing of information, working memory and explicit memory are disturbed, probably to the extent that they require the implementation of strategies to organise the information to be memorized. Finally, in certain tasks, such as those evaluating latent inhibition or negative priming, schizophrenics perform better than normal subjects, suggesting that schizophrenics' cognitive deficit is localised. This profile of memory disorders is compatible with a dysfunction predominating in the frontal and temporo-hippocampal regions. Neuroleptics and anticholinergics have opposite effects on cognitive and mnesic performance, which is improved by the former and aggravated by the latter. The influence of clinical symptoms, positive or negative, institutionalisation of patients and chronic tardive dyskinesia is unclear. Among the theoretical proposals put forward to account for the observed disorders, those relating to a disturbance of the action planning process and to that of the internal representation of context are compatible with the observed memory disorders. All the clinically derived data and those produced by the cognitive and neurosciences indicate a need to reformulate the links between memory, selective attention and evaluation of the relevance of a stimulus, to develop a general model of the reciprocal interactions between cognition and affectivity and to look for the origin of a pathology as complex as schizophrenia, not in a local lesion in an isolated cerebral structure but in a disturbance of the dynamic interactions within a functional, parallel and distributed network of broadly interconnected regions.

Antipsychotic Agents↗
PubMed1977

Levodopa, parkinsonism, and recent memory.

Much controversy has existed concerning behavioral changes attributed to L-dopa treatment in parkinsonian patients. Disagreement existed pertaining to the question of whether improved functioning was temporally limited. The present study proposed to research the shorter and longer range effects of L-dopa onmemory. It was hypothesized that equated nonparkinsonian individuals would perform better than parkinsonian patients on all memory measures, and that shorter range L-dopa would perform better than longer range L-dopa patients. It was also hypothesized that the greater the functional deficiency, and the greater the symptom severity, the poorer memory functioning would be. Level of dosage was hypothesized to have no differential effect on memory functioning. Three groups of 20 subjects were tested. The short term (20 parkinsonian patients on L-dopa for 22 months or less) and the long term (20 parkinsonian patients on L-dopa for 40 months or more) patients were chosen from the neurological clinic at St. Barnabas Hospital, Bronx, N.Y. Testability was assessed by the neurologis and by WAIS Vocabulary performance. The third group consisted of spouses of the patients. All groups were equated with regard to sex, age, education, and where applicable, length of illness, functional status, and symptom severity. The instruments used to measure memory consisted of the Guild Memory Test, the Memory Span for Objects, the Knox Cube, and the Tactile Memory Test. WAIS Vocabulary scaled score was used as a covariate in an analysis of covariance on each of the nine memory subtests. Statistically significant differences were obtained at the .01 level among groups on all measures. Orthogonal comparisons resulted in significant differences at the .01 level between parkinsonian patients and nonparkinsonian subjects on all measures. Short term and long term L-dopa patients differed significantly on six of the nine measures, notably those testing verbal types of memory. Significant correlations were obtained between functional deficiency and eight measures; however, symptom severity correlated with only one measure. None of the memory measures correlated significantly with level of dosage. The major conclusion was reached that all of the initial improvement shown following L-dopa initiation is not sustained permanently; the elevated level of memory functioning appears to be temporally limited.

Humans↗
PubMed1979

Neuropsychological evidence for multiple memory systems.

Neuropsychological data provide strong support for the existence of multiple memory systems. The distinction between short-term memory and long-term memory has been discussed in the experimental literature for some years. More recently it has been argued that the concept of long-term memory is misleading in that it fails to differentiate between semantic memory and episodic/event memory. The independent and selective impairment of multiple memory systems, each with its own functional and structural properties, has been recorded in patients with cerebral lesions and the evidence for impairment of such systems is reviewed. It is argued that the cerebral organization of short-term memory, long-term (non-individual) semantic memory and long-term (individual) event memory is highly differentiated.

Agnosia↗
PubMed1976

Memory recovery after traumatic coma.

Serial memory testings of 108 head injury cases were studied over a two year follow up period. The length of the post-traumatic disorientation period (PTD) was found to be an important factor in the rate of memory recovery. In the first year after injury marked differences were seen in the recovery rates of all four PTD groups, the three short PTD groups (less than one month) finally yielding from 74% to 92% cases (according to the group) with normal memory function, while the long PTD group (more than one month) only produced 45% cases (statistical significance 0.05). During the second year and up to the end of this survey relatively little change in memory status occurred in any of the cases, regardless of their PTD. Any improvement that did occur was at an extremely slow rate. Brain damage was the main cause of memory defect in the long PTD group, while anxiety symptoms had a more important role in the short PTD cases. The shapes of memory recall curves were analysed in recovering patients. Three types of curve were found. The incidence of the shape of the curve also varied according to the PTD time (statistical significance 0.05) between long and short PTD groups. Curve shapes are discussed in terms of memory mechanisms, and a possible prognostic value is suggested. Analysis of test errors indicated not only a defective transfer of material from short term long term memory storage but also in some cases, a more complex mechanism involving inappropriate fixation of attention. Reverberation of memory traces is suggested as being a possible cause of interference in both short and long term memory mechanisms. A marked difference in recall performance between auditory and visual presentation of word lists was found to be a useful lateralising sign.

Adolescent↗
PubMed2025

The effect of scopolamine on memory and attention: a systematic review and meta-analysis.

BACKGROUND: Scopolamine is a muscarinic receptor antagonist and is widely utilized as a "memory-loss model." However, its impact across different memory and attention tasks and using different modes of administration has yet to be clearly evaluated. This systematic review and meta-analysis investigates the effect of scopolamine, across all routes of administration and across different dosages, on memory and attention performance in healthy humans (PROSPERO ID: CRD42024531634). METHODS: Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, we searched (on 20 April 2024) for studies that utilized scopolamine and assessed memory and/or attention. Random-effects meta-analyses were conducted across a range of memory and attention tasks using "Comprehensive Meta-Analysis," Version 3, to evaluate differential pharmacological effects on cognitive tasks between the scopolamine and placebo groups. RESULTS: Forty-six studies fulfilled the inclusion and exclusion criteria. Scopolamine negatively impaired performance on all memory tasks (immediate memory, delayed recall, digit span, Buschke selective reminding task, and recognition memory) and led to slower reaction times for three of the five attention tasks examined (choice reaction time, simple reaction time, and rapid visual information processing) compared to placebo. Scopolamine's negative effect on memory and attention was greater with injectable (e.g., intramuscular, intravenous, and subcutaneous) compared to non-injectable routes of administration (e.g., intranasal, oral, and transdermal). CONCLUSION: This study supports the use of scopolamine as a "memory-loss model," particularly when given by an injectable route of administration. Future clinical trials should evaluate the bioavailability of scopolamine across different routes of administration to ensure therapeutic benefits outweigh any potential adverse cognitive effects.

Humans↗
PubMed1975

Immunological memory function of the T and B cell types: distribution over mouse spleen and lymph nodes.

Spleens from LAF1 mice injected intravenously with sheep erythrocytes (SE) are relatively rich in memory T cells early in the immune response (1 to 3 days) and rich in memory B cells as the response progresses (2 weeks or more). Marked cooperation for the secondary immune response in vitro was obtained by combining 10(6) spleen cells from LAF1 mice, taken 2 days after intravenous priming with SE, with 10(7) spleen cells from day 14 primed mice. The results indicate relative deficiencies in the spleen for B memory cells on days 1 to 2 and for T memory cells on day 14 after priming. Day -14, but not day -2, immune lymph node (LN) cells could replace the day -2 spleen cells (anti-Thy 1.2 sensitive) in the in vitro cooperation with day -14 immune spleen cells. Immune spleen cells taken 4 to 7 days after priming contain more equivalent numbers of B and T memory cells, but 10 to 7 days after transfer of such immune spleen cells without SE into irradiated recipients the T memory cells were again more prominent in lymph node and the B memory cells in spleen as shown by in vitro cooperation studies. These results suggest that during the second week after intravenous injection of SE relatively more T than B memory cells migrate from spleen to lymph node, resulting in an imbalance in the splenic memory cell population favoring B memory cell function.

Animals↗
PubMed1992

Effects of physostigmine on stimulus encoding in a memory-scanning task.

Previous studies of the effects of physostigmine on memory have involved other drugs, a memory that has already been impaired, or both, often with contradictory results. Also, traditional memory tests do not differentiate memory from other task components such as perception and response, and drug effects on these could be mistaken for effects on memory. The present study was designed to investigate the effects of physostigmine alone on normal memory using Sternberg's additive-factor, memory-scanning task, with additional variables to isolate effects on stimulus encoding and response stages. Sixteen volunteers participated, the design was between-groups, and physostigmine or normal saline was given, double-blind, by intravenous infusion for 70 min. The drug had no effect on the memory component of the task, but significantly improved stimulus encoding (P < 0.001). Thus, it is possible that physostigmine improves performance on memory tests by improving perception as well as, or instead of, memory.

Adolescent↗
PubMed1979

Material specific serial memory deficit in adolescent dyslexics.

The present experiment was concerned with an assessment of possible serial, as opposed to general, memory deficit in dyslexia. Previous studies had consistently confounded general and serial memory assessments. Fifteen specifically dyslexic adolescents and 15 normal-reading controls were administered four separate memory tasks. In the general memory for verbal material task they were shown 20 words, each for three seconds, and were then given a deck of 40 word cards and required to pick out the 20 words just seen. In the serial memory version of the verbal task they were again shown 20 words and subsequently required to reproduce the order in which they had been shown. Two comparable (general and serial) procedures were also administered using faces as the to-be-remembered materials. Results showed comparable performances of the dyslexics and controls on both versions of the face memory task and on the general memory version of the words task. On the serial reproduction version of the verbal task, however, dyslexics were found to be significantly impaired relative to controls. Thus, adolescent dyslexics appear to have a memory impairment which is specific for both type of material (verbal) and type of memory (serial). The results are compatible with Orton's (1937) speculation regarding "sequecing" and "memory" in dyslexia and with the view that the defect resides within the neuropsychological processes of the language-dominant hemisphere.

Adolescent↗
PubMed1979

Effects of localised cerebral lesions and dysphasia on verbal memory.

Twenty-nine patients with unilateral left hemisphere lesions, 22 patients with unilateral right hemisphere lesions, and 19 neurological control patients with extracerebral lesions were assessed on verbal memory recall and recognition tests and on a battery of language tests. The left hemisphere group was significantly impaired in memory and language skills. Significant verbal memory impairment was found both in the subgroup of left hemisphere lesion patients whose lesions involved the temporal lobe and in the subgroup whose lesions did not. However, no significant differences between these left hemisphere subgroups' levels of performance on memory tasks emerged, even when dysphasia was taken into account. This study, therefore, fails to support the notion of a specific anatomical correlate of verbal memory impairment within the left hemisphere. Dysphasic subjects were significantly impaired on verbal memory tasks but displayed the same pattern of sensitivity to the effects of word frequency and word concreteness on verbal memory as control subjects, suggesting that the verbal memory of the dysphasic subjects was quantitatively rather than qualitatively impaired. This impairment could not be attributed to deficits in the comprehension or expression of the memory test items, and it is, therefore, proposed that language disturbances may hinder the efficient use of such language based procedures as may subserve verbal memory.

Adult↗
PubMed1975

Memory functions six to nine months after electroconvulsive therapy.

Memory functions after electroconvulsive therapy (ECT) were assessed in 38 former patients who had received bilateral treatment, right unilateral treatment, or hospitalization without ECT six to nine months previously. Results of six different tests of delayed retention and remote memory provided no evidence for persisting memory impairment. Nevertheless, persons who had received bilateral ECT rated their memory as impaired significantly (P less than .05) more often than did persons in the other follow-up groups. Although considerable effort was made to maximize the sensitivity of the memory tests, it is possible that, long after ECT, some impairment of memory remained that was not detected by these tests. Alternatively, it is hypothesized that the impairment of recent and remote memory initially associated with bilateral ECT could cause some persons to become more alert to subsequent memory failures and then to underestimate their memory abilities.

Adult↗