SEARCH · PubMed Health

Results for “memory”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,387 records · Page 77Linked to original sources

PubMed1985

Verbal memory deficits after left temporal lobectomy for epilepsy. Mechanism and intraoperative prediction.

Verbal memory deficits remain a major complication of dominant hemisphere temporal lobectomy for epilepsy. The extent of this deficit was assessed preoperatively and 1 month and 1 year postoperatively with the Wechsler Verbal Memory Scale (WMSV) in 14 adults undergoing left temporal lobectomy. Intraoperative localization of language and verbal memory was also performed by electrical stimulation mapping. The WMSV score decreased an average of 22% at 1 month (13 cases), and 11% at 1 year (10 cases), even though in the majority of cases the medial extent of the resections had been significantly modified as a result of preoperative memory changes in response to intracarotid amobarbital perfusion testing. Memory decline was greater in patients who were not seizure-free, and correlated with the lateral (but not the medial) extent of the resection. The memory deficit could be predicted intraoperatively with 80% accuracy from the relationship of the resection to sites identified by electrical stimulation mapping as essential to naming or input or storage aspects of memory. This technique was applied prospectively in two additional cases with left temporal epileptic foci and complete verbal memory loss with left hemisphere amobarbital inactivation. These resections were tailored to avoid the essential naming and memory sites; the WMSV score increased 1 month postoperatively in both cases. This study identifies a lateral cortical component for verbal memory. Sites essential for that component can be localized intraoperatively with stimulation mapping; when they are spared in a resection, verbal memory deficit following dominant hemisphere temporal lobectomy can be prevented even in high-risk cases.

Adolescent↗

PubMed2003

Assessing absentmindedness: prospective memory complaint and impairment in middle-aged adults.

In two experiments, metamemorial differences between prospective and retrospective memory performance were examined. Participants in Experiment 1 were recruited through newspaper advertisements and comprised middle-aged women who experienced exceptional problems in prospective remembering. Experiment 2 involved self-reporters and nonreporters of retrospective memory problems, who were selected from a large population-based sample of middle-aged adults. In both experiments, memory performance was assessed by using a variety of tasks, including five retrospective memory tasks and three prospective memory tasks that varied in level of realism and retrieval support. In both experiments, there were selective differences in memory performance, so that participants who experienced (retrospective or prospective) memory problems showed impaired performance in prospective, but not in retrospective, memory tasks. These findings suggest that memory for future intentions provides a more sensitive task criterion than does memory for past events for assessing individual differences in self-reports of episodic memory problems. Task-specific differences in reliance on frontally mediated executive processes might underlie these differences.

Adult↗

PubMed2000

Lymphotoxin-alpha-dependent spleen microenvironment supports the generation of memory B cells and is required for their subsequent antigen-induced activation.

Lymphotoxin alpha-deficient (LTalpha-/-) mice show dramatically reduced IgG responses after either primary or secondary immunizations with sheep red blood cells (SRBC). When splenocytes from SRBC-primed wild-type donor mice were infused into irradiated naive wild-type recipient mice, they generated a robust memory IgG response, but not when infused into LTalpha-/- recipients, indicating that the microenvironment that develops in LTalpha-/- mice is incompetent to support the activation of this memory response. When irradiated wild-type mice were reconstituted with splenocytes from primed LTalpha-/- donors and then challenged with the same immunizing Ag, no memory response was observed, indicating further that memory cells could not be generated in the LTalpha-/- environment. To address which lymphocyte subsets were impaired in the LTalpha-/- mice, we performed reconstitution experiments using a hapten/carrier system and T cells and B cells from different primed donors. There was no detectable defect in either the generation or expression of memory T cells from LTalpha-/- donors. In contrast, B cells were not primed for memory in the microenvironment of LTalpha-/- mice. Additionally, primed wild-type memory B cells could not express a memory IgG response in the LTalpha-/- microenvironment. Thus, splenic white pulp structure, which depends on the expression of LTalpha for its development and maintenance, is needed to support the generation of memory B cells and to permit existing memory B cells to express an isotype switched memory Ig response following antigenic challenge.

Animals↗

PubMed2003

Intrinsic differences in the proliferation of naive and memory human B cells as a mechanism for enhanced secondary immune responses.

Humoral immune responses elicited after secondary exposure to immunizing Ag are characterized by robust and elevated reactivity of memory B cells that exceed those of naive B cells during the primary response. The mechanism underlying this difference in responsiveness of naive vs memory B cells remains unclear. We have quantitated the response of naive and memory human B cells after in vitro stimulation with T cell-derived stimuli. In response to stimulation with CD40 ligand alone or with IL-10, both IgM-expressing and Ig isotype-switched memory B cells entered their first division 20-30 h earlier than did naive B cells. In contrast, the time spent traversing subsequent divisions was similar. Consistent with previous studies, only memory cells differentiated to CD38(+) blasts in a manner that increased with consecutive division number. These differentiated CD38(+) B cells divided faster than did CD38(-) memory B cell blasts. Proliferation of CD40 ligand-stimulated naive B cells as well as both CD38(+) and CD38(-) cells present in cultures of memory B cells was increased by IL-10. In contrast, IL-2 enhanced proliferation of CD38(-) and CD38(+) memory B cell blasts, but not naive cells. Thus, memory B cells possess an intrinsic advantage over naive B cells in both the time to initiate a response and in the division-based rate of effector cell development. These differences help explain the accelerated Ab response exhibited by memory B cells after secondary challenge by an invading pathogen, a hallmark of immunological memory.

ADP-ribosyl Cyclase↗

PubMed2005

CD8 cell division maintaining cytotoxic memory occurs predominantly in the bone marrow.

Long-term persistence of Ag-experienced CD8 cells, a class of T lymphocytes with cytotoxic function, contributes to immunological memory against intracellular pathogens. After Ag clearance, memory CD8 cells are maintained over time by a slow proliferation, primarily cytokine driven. In this article, we show that the bone marrow (BM) is the crucial organ where such basal division of memory CD8 cells occurs. BM memory CD8 cells contain a higher percentage of proliferating cells than their corresponding cells in either spleen or lymph nodes from C57BL/6 mice. This occurs both in the case of memory-phenotype CD44(high) CD8 cells and in the case of Ag-specific memory CD8 cells. Importantly, the absolute number of Ag-specific memory CD8 cells dividing in the BM largely exceeds that in spleen, lymph nodes, liver, and lung taken together. In the BM, Ag-specific memory CD8 cells express lower levels of CD127, i.e., the alpha-chain of IL-7R, than in either spleen or lymph nodes. We interpret these results as indirect evidence that Ag-specific memory CD8 cells receive proliferative signals by IL-7 and/or IL-15 in the BM and propose that the BM acts as a saturable "niche" for the Ag-independent proliferation of memory CD8 cells. Taken together, our novel findings indicate that the BM plays a relevant role in the maintenance of cytotoxic T cell memory, in addition to its previously described involvement in long-term Ab responses.

Adoptive Transfer↗

PubMedDate not supplied

Working memory and older adults: implications for occupational therapy.

Atkinson and Shiffrin's (1968) modal model of memory is still commonly used by rehabilitation professionals to evaluate memory impairment in older adults. However, research to date has been unable to indicate that short-term memory declines with age. These findings have led some rehabilitation professionals to mistakenly conclude that short-term memory is not affected by the aging process. This article reviews both the traditional concept of short-term memory, as outlined by Atkinson and Shiffrin, and the more recent conceptualization of short-term memory in terms of Baddeley and Hitch's (1974) model of working memory. The implications of the concept of working memory has implications for occupational therapy interventions for older adults. For example, clients with dementia may experience difficulties in performing tasks that require drawing inferences. Similarly, language that contains vague references may present problems for these clients. In addition, changes in working memory in older adults suggest that they may experience difficulties with medication management and what Rule, Milke, and Dobbs (1992) called wayfinding. Therefore, evaluations of working memory would provide a better indication of older adults' memory performance than the modal model.

Aged↗

PubMedDate not supplied

[Heroin abuse, autobiographical memory and depression].

The early psychiatric interviews with opiate addicts are characterized by three features: 1) the patient has a very factual and objective conversation, 2) the evaluation of the autobiographical memory is very difficult, 3) there is a high prevalence of affective disorders responsible for an impairment in cognitive functions. Therefore we have two aims: First, to compare episodic and semantic autobiographical memory in opiate addicts and healthy controls. Autobiographical memory is the knowledge a person has about oneself and his past. Personal semantic memory is the knowledge of the biographical facts, general knowledge and beliefs about oneself. Autobiographical episodic memory concerns recollections of personal events clearly delineated in time and space. Second, to estimate the impact of depression on the ability to produce autobiographical recollection in a population of opiatre addicts. Participants were consecutive attenders of a methadone outpatient clinic who are multiple drug dependent patients consuming mainly heroine. The first investigation took place in entry and after two months. We have recruited 21 patients with a mean duration of intoxication of 11 years. Ten of these patients have been investigated again after 2 months and 8 of them have been included in a methadone maintenance program. The patients'investigation comprised two parts: first, the evaluation of autobiographical memory (only assessed at entry of the study) with an autobiographical fluency test and the semi-structured autobiographical memory interview of Kopelman; second, the psychiatric assessment included self-rating questionnaires and observer-rating questionnaires. Opiate addicts showed a decrease in episodic autobiographical memory but an increase in semantic affective memory and objective modalization. In the fluency test, there was no difference in the number of evoked items between opiate addicts and healthy controls. The educational level influences several results. The possible explanations of these results are the action of the toxic products and a particular psychic functioning. The lack of correlation between autobiographical memory and affective disorder suggests the implication of the drugs in the emergence of memory deficits. The improvement of depressive symptomatology after two months occurring without psychotropic drugs suggests the transient feature of depression and emphasises on non-pharmacological aspects of treatment.

Adult↗

PubMed2000

Remote episodic memory deficits in patients with unilateral temporal lobe epilepsy and excisions.

The nature of remote memory impairment in patients with medial temporal lobe damage is the subject of some debate. While some investigators have found that retrograde amnesia in such patients is temporally graded, with relative sparing of remote memories (Squire and Alvarez, 1995), others contend that impairment is of very long duration and that remote memories are not necessarily spared (Sanders and Warrington, 1971; Nadel and Moscovitch, 1997). In this study, remote memory was assessed in 25 patients with unilateral temporal lobe epilepsy and 22 non-neurologically impaired controls using the Autobiographical Memory Interview (Kopelman et al., 1989). Results indicate that patients have impaired personal episodic memory but intact personal semantic memory. The impairment extends even to the most remote time periods in early childhood, long before seizure onset in many patients. As well, patients awaiting temporal lobectomy for control of seizures perform as poorly as those who have already undergone resective surgery. These results support the hypothesis that temporal lobe damage or dysfunction, caused by recurrent seizures or surgical excision, results in extensive retrograde amnesia for personal episodic memories. Interestingly, patients with radiological evidence of hippocampal sclerosis were not significantly more impaired than those without obvious sclerosis. These results indicate that even minimal damage to medial temporal lobes results in significant impairment to autobiographical episodic memory. These findings are more compatible with a memory loss or retrieval deficit rather than a consolidation account of remote memory impairment.

Adult↗

PubMed2001

A model of the interaction between mood and memory.

This paper investigates a neural network model of the interaction between mood and memory. The model has two attractor networks that represent the inferior temporal cortex (IT), which stores representations of visual stimuli, and the amygdala, the activity of which reflects the mood state. The two attractor networks are coupled by forward and backward projections. The model is however generic, and is relevant to understanding the interaction between different pairs of modules in the brain, particularly, as is the case with moods and memories, when there are fewer states represented in one module than in the other. During learning, a large number of patterns are presented to the IT, each paired with one of two mood states represented in the amygdala. The recurrent connections within each module, the forward connections from the memory module to the amygdala, and the backward connections from the amygdala to the memory module, are associatively modified. It is shown how the mood state in the amygdala can influence which memory patterns are recalled in the memory module. Further, it is shown that if there is an existing mood state in the amygdala, it can be difficult to change it even when a retrieval cue is presented to the memory module that is associated with a different mood state. It is also shown that the backprojections from the amygdala to the memory module must be relatively weak if memory retrieval in the memory module is not to be disrupted. The results are relevant to understanding the interaction between structures important in mood and emotion (such as the amygdala and orbitofrontal cortex) and other brain areas involved in storing objects and faces (such as the inferior temporal visual cortex) and memories (such as the hippocampus).

Affect↗

PubMed2003

[Autobiographical memory in aging].

Episodic memory deficits are characteristic of old subjects. However, few results concern studies of autobiographical memory, one of the most essential part of human memory. Usually remote, but not recent, memory is regarded as preserved in aging. This phenomenom is well known as the Ribot's law. We briefly present the recent models of autobiographical memory and we detail the different aspects of aging on the two components, either episodic or semantic, of autobiographical memory. The data are reviewed with respect to the different kinds of autobiographical memory assessments : cue-words technique, autobiographical verbal fluency and interview. In addition, we present the results from novel autobiographical memory tasks specially designed to be more valid and reliable than the previous neuropsychological tools by assessing the contribution of episodic and semantic memory systems to autobiographical performance viaexperimental paradigms (remember/know). This review shows that the Ribot's law is not confirmed in aging by contrast with Alzheimer's disease. Indeed, in older subjects, the performances on episodic autobiographical memory tests diminish with time interval, with a clear recency effect. Moreover, the episodic, but not the semantic, component of autobiographical memory is significantly altered in aging.

Aged↗

PubMed2005

Post-traumatic stress disorder and memory: prescient medicolegal testimony at the International War Crimes Tribunal?

The nature of remembrance of traumatic events has been particularly controversial during the past decade as vigorous new research has reshaped thinking about trauma and memory. Memory alterations in traumatized individuals have been investigated within both theoretical and biological frameworks. There are different types of memory, and empirical studies have associated post-traumatic stress disorder (PTSD) with a simultaneous weakening and a strengthening of memory. Memory deficiencies in PTSD have been found to be related to problems in new learning (explicit memory), but other specific deficiencies are unvalidated. Recently, accuracy of memory has received particular scrutiny because considerable importance is attached to victims' recollections. In 1998, at the International War Crimes Tribunal in The Hague, The Netherlands, a Bosnian-Croatian soldier was tried for aiding and abetting the rape of a Muslim woman. The defendant's lawyers suggested that the woman's memory was inaccurate, having been adversely affected by her traumatic experiences, and that the defendant whom she identified was not present during her interrogation and abuse. The prosecution disagreed and argued that memories of traumatic experiences in individuals with PTSD are characteristically hyperaccessible. Expert witnesses on both sides were brought in to provide medicolegal testimony about the scientific parameters of stress and its long-term effects on brain regions associated with memory. With the expert witness discussion as background, this article reviews the most recent research about the nature of memory in the aftermath of trauma and the politics of psychological trauma and the law.

Bosnia and Herzegovina↗

PubMed1993

Role of the amygdala, hippocampus and entorhinal cortex in memory consolidation and expression.

1. Experiments using localized microinfusions of specific agonists and antagonists of neurotransmitter receptors have shown that the amygdala, hippocampus, medial septum and entorhinal cortex are involved in memory consolidation, storage and expression. The data are consistent with observations derived from lesion studies suggesting a role for these structures in memory processes, but permit many additional conclusions concerning the mechanisms involved and their timing. 2. Memories are initially processed by glutamatergic N-methyl-D-aspartate (NMDA) receptors in amygdala, hippocampus and medial septum, which are sensitive to amino-phosphono valerate (AP5). Memory of inhibitory avoidance is processed by the three structures; memory of habituation to a novel environment is processed only by the hippocampus. At the time of consolidation, immediately after training, gamma-aminobutyrate type A (GABA-A) receptors, modulated by endogenous benzodiazepines, play an inhibitory role, and cholinergic muscarinic and beta-noradrenergic transmission play a modulatory role. 3. From 90 to 180 min after training, memories are blocked by cyano-nitro-quinoxalinedione (CNQX) given into the amygdala, septum and hippocampus. CNQX blocks non-NMDA glutamatergic receptors. Also between 90 and 180 min after training, memory of the habituation and inhibitory avoidance tasks is blocked by the infusion of AP5 or of the GABA-A agonist, muscimol, into the entorhinal cortex. This late post-training intervention of the entorhinal cortex is essential for the integration of successively acquired memories, and occurs in response to the simultaneous activation of CNQX-sensitive synapses in amygdala and hippocampus. 4. The expression of memory is blocked by the infusion of CNQX, at the time of testing, into the amygdala and hippocampus (inhibitory avoidance), into the hippocampus but not the amygdala (habituation), or into the entorhinal cortex (for the two tasks). Since consolidation is blocked by AP5 infused into these structures (see above), the data agree with the hypothesis that memories are mediated by (or actually consist of) long-term potentiation (LTP) in these areas of the brain. LTP induction is blocked by AP5 and LTP expression is blocked by CNQX. It is possible that, at the time of memory expression, the entorhinal cortex is an output of the amygdala and hippocampus.

2-Amino-5-phosphonovalerate↗

PubMed1994

Neuronal activity in human lateral temporal cortex during serial retrieval from short-term memory.

Neuronal activity was recorded extracellularly from 20 populations in the lateral cortex of the left anterior temporal lobe of 11 patients undergoing awake craniotomy for epilepsy, during an input-distraction-retrieval measure of recent verbal memory that also included two later successive retrievals of the same information after additional distracting tasks. Changes in activity were determined for each 1 sec epoch in three major comparisons: (1) the same visual cues used for naming an input to recent memory, naming without a memory component, and a spatial matching task; (2) memory input (MI), distraction (S), and initial cued retrieval (R1) from memory, where object naming was the input to memory and naming of other objects the distractors; (3) initial retrieval (R1) and the two subsequent serial retrievals of the same information (R2, R3). Control comparisons were also made with serial naming and viewing of blank slides, and repeated naming of the same objects. In comparison 1, 13 of the 20 populations showed consistently increased activity during memory input ("memory units"); two others showed changes during language measures. In comparison 2, a significant proportion of all 20 populations, and the 13 memory units considered alone showed increased activity in initial epochs of MI and R1, confirming earlier findings of increased lateral temporal neuronal activity at memory entry and initial retrieval. In comparison 3, a significant proportion of the memory units showed increased activity in early epochs of R1 and decreased activity in late epochs of R3. This decrease in populations with increased activity at R1 was also evident when R1 was compared to R2 or R2 to R3.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1995

Mucosal memory B cells retain the ability to produce IgM antibodies 2 years after oral immunization.

In recent studies we have demonstrated that immunological B- and T-cell memory may be stimulated effectively by oral immunization, simply by admixing protein antigens with cholera toxin (CT) adjuvant. Here we extend information by employing a hapten-carrier system allowing us to separate B- and T-cell memory and to evaluate the requirement of memory T cells for effective reactivation of mucosal memory B cells. We found that 2 weeks following oral priming immunizations with dinitrophenyl-keyhole limpet haemocyanin (DNP-KLH) plus CT adjuvant, significant serum anti-DNP antibodies of IgG, IgA and IgM immunoglobulin classes were demonstrated. However, after 2 years only IgM anti-DNP antibodies could still be detected in serum. When memory lymphocytes were isolated from these mice, from both systemic and gut-associated lymphoid tissues, and challenged with antigen in vitro, vigorous IgM, but no IgG or IgA, anti-DNP production was observed. By contrast, when the DNP-KHL-primed memory mice were challenged in vivo by an oral booster immunization with DNP-KLH plus CT adjuvant, strong systemic IgG and local mucosal IgA anti-DNP responses were recorded, while IgM anti-DNP production was poor. Moreover, the mucosal memory B cells from DNP-KHL-immunized mice were more responsive in vivo to an oral booster immunization with the carrier-specific antigen, DNP-KLH, compared to that provided by an unrelated carrier, DNP-human serum albumin (HSA), which gave only poor mucosal and systemic anti-DNP B-cell responses. Taken together our data suggest that mucosal memory B cells are recirculating cells that have retained their ability to produce IgM antibodies and, therefore, have not undergone switch differentiation involving gene rearrangements with constant mu-chain deletions. Furthermore, mucosal B-cell memory and CD4+ T-cell memory are closely interconnected phenomena, requiring both components for effective expression and probably also for maintenance of immunological memory in the mucosal immune system.

Administration, Oral↗

PubMed1997

Acute nicotine interactions with nicotinic and muscarinic antagonists: working and reference memory effects in the 16-arm radial maze.

In the 8-arm radial maze and other tests, acute nicotine administration has been found to improve memory performance significantly, whereas acute administration of the nicotinic antagonist mecamylamine has been found to impair memory performance. However, questions remain concerning the behavioral and pharmacological nature of acute nicotine effects on memory. In the current studies, we examined acute nicotine effects on working and reference memory in a 16-arm radial maze. In the first study, nicotine caused a significant improvement in working memory but not in reference memory. The muscarinic antagonist scopolamine caused significant deficits in working memory but not in reference memory. Nicotine did not significantly attenuate the scopolamine-induced deficit. In the second study, with rats trained to near-perfect performance, a low dose of mecamylamine (1.25 mg/kg) caused a significant working memory impairment in the 16-arm maze. This deficit was significantly attenuated by concurrent acute administration of nicotine. These studies show that acute nicotine, like chronic nicotine, preferentially improves working compared with reference memory in the radial-arm maze. Mecamylamine can impair working memory performance in the 16-arm maze at low doses which are less likely to have effects at N-methyl-D-aspartate receptors. Nicotine can selectively reverse mecamylamine-induced deficits.

Animals↗

PubMedDate not supplied

[Effects of cognitive aging on memory performances].

PSYCHOLOGY OF AGING: This article sums up studies on influence of normal aging in memory. Aging is a process involving many dimensions: Psychological, Biological and Social. These elements interact with each other and needed to be considered in the description of human memory aging. COGNITIVE APPROACH OF HUMAN MEMORY: Moreover, researches on human memory have been conducted within the framework of current theoretical views of memory. The present review provides an outline of the cognitive neuropsychology models of memory, its nature, components and organization. CLINICAL APPROACH OF AGING AND MEMORY, CONSEQUENCES: This introduction may help the reader to understand more clearly empirical evidence of age-related differences in memory and attentional functioning. In closing, the human factors psychologists must be take in account while adopting a global approach of the understanding of memory aging. Psychological field provides a complete structure for assessing human being and is helpful before to conclude between normal or pathological memory aging.

Adult↗

PubMed1993

Hippocampal CRF, NE, and NMDA system interactions in memory processing in the rat.

In the present study, we investigated the neural mechanisms of corticotropin-releasing factor (CRF) and the interactions among CRF, norepinephrine (NE), and N-methyl-D-aspartate (NMDA) systems in the dentate gyrus (DG) of hippocampus in modulating the memory process of rats. One-way passive avoidance task was adopted. Results indicated that CRF (80 ng), when directly injected into the DG, consistently and significantly enhanced memory retention in rats. The noradrenergic neurotoxin DSP-4, at a high dose (4 micrograms), impaired memory. DSP-4 at a moderate dose (2 micrograms), which did not affect retention alone, antagonized the memory-enhancing effect of CRF. Similarly, the beta-adrenergic antagonist propranolol, at a high dose (8 micrograms), reduced retention. At a low dose (80 ng), which did not markedly affect retention by itself, propranolol also prevented the memory-improving effect of CRF. Moreover, direct NE infusions to the DG significantly improved retention performance in a dose-sensitive manner. Coadministration of CRF and NE did not further enhance retention. These results together suggest that CRF and NE facilitated memory probably through the same instead of independent mechanisms. In contrast, the selective NMDA receptor antagonists 2-amino-5-phosphonopentanoate (AP5) and MK801, at high doses markedly impaired memory retention (0.8 and 3.2 micrograms for AP5, 2 and 10 micrograms for MK801). At a dose of MK801 that did not significantly alter retention alone (80 ng), it completely blocked the memory-facilitating effect of CRF. These results indicate that CRF enhanced memory indirectly through NMDA receptor mediation also. Finally, MK801 at 80 ng also successfully antagonized the memory-facilitating effect of NE in the DG. We have demonstrated that MK801, at the dose chosen for interaction studies, did not markedly alter locomotor activity. These results together suggest that CRF, through a presynaptic facilitation mechanism, possibly facilitates NE release in the DG; increased NE release and stimulation of beta-adrenergic receptors in the DG result in NMDA receptor activations in the same area. This sequence of events enhance the memory consolidation process in the hippocampus and explained the neural mechanism of CRF in facilitating retention performance in rats. The same neuropeptide/neurotransmitter interactions may have other physiological and neuropathological implications.

Adrenergic Agents↗

PubMed1998

Amygdala modulation of multiple memory systems: hippocampus and caudate-putamen.

A series of five experiments examined the differential mnemonic roles of the hippocampus and caudate-putamen and the modulatory influence of the amygdala on hippocampal and caudate-putamen memory processes. Findings indicate that (a) posttraining intrahippocampal injections of amphetamine selectively enhance memory in a hidden platform water maze task, (b) posttraining intracaudate injections of amphetamine selectively enhance memory in a visible platform water maze task, (c) posttraining intra-amygdala injections of amphetamine enhance memory in both water maze tasks, (d) preretention intrahippocampal lidocaine injections block expression of the memory enhancing effects of posttraining intrahippocampal amphetamine injections in the hidden platform task, (e) preretention intracaudate lidocaine injections block expression of the memory enhancing effects of posttraining intracaudate amphetamine injections in the visible platform task, (f) preretention intra-amygdala lidocaine injections do not block the memory enhancing effect of posttraining intra-amygdala amphetamine injections on either task, (g) in the hidden platform task, posttraining intrahippocampal, but not intracaudate, lidocaine injections block the memory enhancing effects of posttraining intra-amygdala amphetamine, (h) in the visible platform task, posttraining intracaudate, but not intrahippocampal, lidocaine injections block the memory enhancing effects of posttraining intra-amygdala amphetamine. The findings indicate a double dissociation between the roles of the hippocampus and caudate-putamen in memory and suggest that the amygdala exerts a modulatory influence on both the hippocampal and caudate-putamen memory systems.

Adrenergic Uptake Inhibitors↗