Top-down signal from prefrontal cortex in executive control of memory retrieval.

Knowledge or experience is voluntarily recalled from memory by reactivation of the neural representations in the cerebral association cortex. In inferior temporal cortex, which serves as the storehouse of visual long-term memory, activation of mnemonic engrams through electric stimulation results in imagery recall in humans, and neurons can be dynamically activated by the necessity for memory recall in monkeys. Neuropsychological studies and previous split-brain experiments predicted that prefrontal cortex exerts executive control upon inferior temporal cortex in memory retrieval; however, no neuronal correlate of this process has ever been detected. Here we show evidence of the top-down signal from prefrontal cortex. In the absence of bottom-up visual inputs, single inferior temporal neurons were activated by the top-down signal, which conveyed information on semantic categorization imposed by visual stimulus-stimulus association. Behavioural performance was severely impaired with loss of the top-down signal. Control experiments confirmed that the signal was transmitted not through a subcortical but through a fronto-temporal cortical pathway. Thus, feedback projections from prefrontal cortex to the posterior association cortex appear to serve the executive control of voluntary recall.     

乘除形态学联想记忆及其性能分析

形态学联想记忆是一类新颖的人工神经网络,但是它的异联想记忆效果较差.针对这个问题,基于互补的思想,提出一种形态学联想记忆方法,称为乘除形态学联想记忆.文中分析了乘除形态学联想记忆方法完全回忆记忆的条件及其噪声性质.分析和实验表明,这种方法对异联想效果显著,并具有一定的抗噪声鲁棒性,在一些情况下,能够取得更好的异联想效果.     

Updating verbal and visuospatial working memory： Are the processes parallel？

The current study compared the processes of updating verbal and visuospatial working memory （WM） and examined the roles of central executive and slave systems in working memory updating tasks, by changing the number of items updated simultaneously to manipulate the load on central executive. Experiment 1 used the verbal WM updating task, and the results validated the efficiency of the paradigm to manipulate the load on central executive. Experiment 2 employed the verbal WM updating task, with the articulatory suppression task to interfere with the phonological loop. The results supported the study by Morris and Jones, revealing that the central executive system played an important role in the updating component of verbal WM, while the phonological loop was responsible for the serial recall component. Experiment 3 employed the visuospatial WM updating task, with the spatial tapping task to interfere with the visuospatial sketchpad. The results suggested that the visuospatial sketchpad and the central executive together dealt with the updating component, while the visuospatial sketchpad was responsible for the serial recall component by itself. These results are consistent with the findings that visuospatial sketchpad has close links with central executive, while the phonological loop is separated from the central executive. It suggests that updating visuospatial and verbal WM are not two parallel processes.     

What can false memory tell us about memory impairments in Alzheimer’s disease?

The range of memory impairments associated with Alzheimer’s disease (AD) has been a focus for psychological and clinical re-searchers for many years. In addition to investigations of AD patients’ veridical memory using traditional recognition memory tasks, a number of recent studies have focused on false memories to reveal the underlying causes of memory impairment in AD. Studies comparing illusory memories between AD patients and healthy older people have revealed various differences in memory deficits between the development of AD and the typical aging processes. Here, we review 3 types of memory illusions tested in AD patients: associative memory illusions, fluency-based false memories and source memory errors. By comparing AD patients with healthy older adults, we sought to analyze the mechanisms underlying AD-related memory impairments at different stages of memory processing, including encoding, retrieval and monitoring. This comparison revealed that AD patients exhibit an impaired ability to establish and utilize gist representations at the encoding stage and impairments in processing on the basis of familiarity and recollection at the retrieval stage. Consequently, patients with AD have access to less information when making memory judgments. As a result, they become more susceptible to the effects of item fluency, which can be manipulated during the retrieval stage. Furthermore, with impaired source memory monitoring abilities, the capacity of AD patients to suppress memory illusions is compromised. Based on these findings, we propose that the study of false memories constitute a critical tool for elucidating the memory impairments involved in AD. Further explorations of these memory impairments will have practical significance for the diagnosis and treatment of AD in the future.     

分配注意对短时记忆编码和提取的影响

以大学生为被试,采用分配注意范式探讨了短时记忆编码和提取所需的注意资源。研究发现：与集中注意相比,编码阶段进行第二作业导致记忆成绩显著降低,而提取阶段进行第二作业则对记忆成绩没有影响。自由回忆和顺序回忆的结果一致。本研究表明,短时记忆编码是需要较多注意资源的控制加工,而短时记忆提取则是相对无需注意资源的自动加工。这与当前关于长时记忆的研究结果类似,而与早期以第二作业成绩为测量指标的短时记忆研究结果有所不同。     

Alpha-CaMKII-dependent plasticity in the cortex is required for permanent memory

Cortical plasticity seems to be critical for the establishment of permanent memory traces. Little is known, however, about the molecular and cellular processes that support consolidation of memories in cortical networks. Here we show that mice heterozygous for a null mutation of alpha-calcium-calmodulin kinase II (alpha-CaMKII+/-) show normal learning and memory 1-3 days after training in two hippocampus-dependent tasks. However, their memory is severely impaired at longer retention delays (10-50 days). Consistent with this, we found that alpha-CaMKII+/- mice have impaired cortical, but not hippocampal, long-term potentiation. Our results represent a first step in unveiling the molecular and cellular mechanisms underlying the establishment of permanent memories, and they indicate that alpha-CaMKII may modulate the synaptic events required for the consolidation of memory traces in cortical networks.     

Memory for places learned long ago is intact after hippocampal damage.

The hippocampus is part of a system of structures in the medial temporal lobe that are essential for memory. One influential view of hippocampal function emphasizes its role in the acquisition and retrieval of spatial knowledge. By this view, the hippocampus constructs and stores spatial maps and is therefore essential for learning and remembering places, including those learned about long ago. We tested a profoundly amnesic patient (E.P.), who has virtually complete bilateral damage to the hippocampus and extensive damage to adjacent structures in the medial temporal lobe. We asked him to recall the spatial layout of the region where he grew up, from which he moved away more than 50 years ago. E.P. performed as well as or better than age-matched control subjects who grew up in the same region and also moved away. In contrast, E.P. has no knowledge of his current neighbourhood, to which he moved after he became amnesic. Our results show that the medial temporal lobe is not the permanent repository of spatial maps, and support the view that the hippocampus and other structures in the medial temporal lobe are essential for the formation of long-term declarative memories, both spatial and non-spatial, but not for the retrieval of very remote memories, either spatial or non-spatial.     

高校少数民族女生身心特点现状及发展研究

随着国家高考政策向少数民族倾斜力度增大,越来越多的少数民族学生走进了大学校园,少数民族女大学生的身心健康及发展成为高校体育教育的重点问题.通过对具体高校7266名女大学生的身体素质进行测试,结果显示：少数民族女大学生身体素质较汉族学生好,但呈现出强烈的民族意识、脆弱的心理素质、生活上的不适感等特点.因此应采取尊重民族风俗、推广民族体育项目、鼓励女大学生进行有氧健美操运动等方式进行调节.     

Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval

'New' memories are initially labile and sensitive to disruption before being consolidated into stable long-term memories. Much evidence indicates that this consolidation involves the synthesis of new proteins in neurons. The lateral and basal nuclei of the amygdala (LBA) are believed to be a site of memory storage in fear learning. Infusion of the protein synthesis inhibitor anisomycin into the LBA shortly after training prevents consolidation of fear memories. Here we show that consolidated fear memories, when reactivated during retrieval, return to a labile state in which infusion of anisomycin shortly after memory reactivation produces amnesia on later tests, regardless of whether reactivation was performed 1 or 14 days after conditioning. The same treatment with anisomycin, in the absence of memory reactivation, left memory intact. Consistent with a time-limited role for protein synthesis production in consolidation, delay of the infusion until six hours after memory reactivation produced no amnesia. Our data show that consolidated fear memories, when reactivated, return to a labile state that requires de novo protein synthesis for reconsolidation. These findings are not predicted by traditional theories of memory consolidation.     

Can the memory of an object be enhanced by imagining its loss?

Previous investigations examining salient memories have demonstrated that personal memories that are important to individuals and contain emotional information are better remembered than neutral events.Using behavioral and brain-imaging experiments,the present studies explored whether the previous finding was applicable imagined loss.In a behavioral experiment,a free recall paradigm was used to compare the memory performance of individuals who imagined loss with that of individuals who imagined importance.The superior memory performance conferred by imagining loss was constrained to ordinary items of low to medium importance and did not generalize to vital items.Moreover,brain imaging evidence revealed that the activation in certain brain regions was stronger when participants were imagining the loss of ordinary items of low to medium importance compared to vital items.These brain regions included cognitive effort-related areas(such as the parietal cortex and middle prefrontal cortex) and areas related to emotional experiences and emotion-related memories(such as the amygdala,parahippocampal gyrus,and posterior cingulate gyrus).Our study provides a new way of exploring the superior memory performance when imagining loss and enriches the literature on memory enhancement by contributing to a deeper understanding of the psychological mechanisms related to the imagining of vital losses.     

Visual place learning in Drosophila melanogaster

The ability of insects to learn and navigate to specific locations in the environment has fascinated naturalists for decades. The impressive navigational abilities of ants, bees, wasps and other insects demonstrate that insects are capable of visual place learning, but little is known about the underlying neural circuits that mediate these behaviours. Drosophila melanogaster (common fruit fly) is a powerful model organism for dissecting the neural circuitry underlying complex behaviours, from sensory perception to learning and memory. Drosophila can identify and remember visual features such as size, colour and contour orientation. However, the extent to which they use vision to recall specific locations remains unclear. Here we describe a visual place learning platform and demonstrate that Drosophila are capable of forming and retaining visual place memories to guide selective navigation. By targeted genetic silencing of small subsets of cells in the Drosophila brain, we show that neurons in the ellipsoid body, but not in the mushroom bodies, are necessary for visual place learning. Together, these studies reveal distinct neuroanatomical substrates for spatial versus non-spatial learning, and establish Drosophila as a powerful model for the study of spatial memories.     

一种混合模糊联想记忆网络

本文改进了Ｋｏｓｋｏ．Ｂ提出的最大最小联想记忆网络的模糊Ｈｅｂｂ关系编码规则,给出了一种新的学习算法,新算法克服了Ｋｏｓｋｏ．Ｂ算法的缺陷,在一定条件下,本文的学习算法能将模式对完整地联想出来．另外,本文在分析网络的容错性及稳定性的基础上,提出了一种五层混合模糊联想记忆网络,五层混合网络具有良好的联想容错能力．实验结果表明,本文的学习算法及混合网络是有效的．     

Optogenetic stimulation of a hippocampal engram activates fear memory recall

A specific memory is thought to be encoded by a sparse population of neurons. These neurons can be tagged during learning for subsequent identification and manipulation. Moreover, their ablation or inactivation results in reduced memory expression, suggesting their necessity in mnemonic processes. However, the question of sufficiency remains: it is unclear whether it is possible to elicit the behavioural output of a specific memory by directly activating a population of neurons that was active during learning. Here we show in mice that optogenetic reactivation of hippocampal neurons activated during fear conditioning is sufficient to induce freezing behaviour. We labelled a population of hippocampal dentate gyrus neurons activated during fear learning with channelrhodopsin-2 (ChR2) and later optically reactivated these neurons in a different context. The mice showed increased freezing only upon light stimulation, indicating light-induced fear memory recall. This freezing was not detected in non-fear-conditioned mice expressing ChR2 in a similar proportion of cells, nor in fear-conditioned mice with cells labelled by enhanced yellow fluorescent protein instead of ChR2. Finally, activation of cells labelled in a context not associated with fear did not evoke freezing in mice that were previously fear conditioned in a different context, suggesting that light-induced fear memory recall is context specific. Together, our findings indicate that activating a sparse but specific ensemble of hippocampal neurons that contribute to a memory engram is sufficient for the recall of that memory. Moreover, our experimental approach offers a general method of mapping cellular populations bearing memory engrams.     

Learning-related feedforward inhibitory connectivity growth required for memory precision

In the adult brain, new synapses are formed and pre-existing ones are lost, but the function of this structural plasticity has remained unclear. Learning of new skills is correlated with formation of new synapses. These may directly encode new memories, but they may also have more general roles in memory encoding and retrieval processes. Here we investigated how mossy fibre terminal complexes at the entry of hippocampal and cerebellar circuits rearrange upon learning in mice, and what is the functional role of the rearrangements. We show that one-trial and incremental learning lead to robust, circuit-specific, long-lasting and reversible increases in the numbers of filopodial synapses onto fast-spiking interneurons that trigger feedforward inhibition. The increase in feedforward inhibition connectivity involved a majority of the presynaptic terminals, restricted the numbers of c-Fos-expressing postsynaptic neurons at memory retrieval, and correlated temporally with the quality of the memory. We then show that for contextual fear conditioning and Morris water maze learning, increased feedforward inhibition connectivity by hippocampal mossy fibres has a critical role for the precision of the memory and the learned behaviour. In the absence of mossy fibre long-term potentiation in Rab3a(-/-) mice, c-Fos ensemble reorganization and feedforward inhibition growth were both absent in CA3 upon learning, and the memory was imprecise. By contrast, in the absence of adducin 2 (Add2; also known as β-adducin) c-Fos reorganization was normal, but feedforward inhibition growth was abolished. In parallel, c-Fos ensembles in CA3 were greatly enlarged, and the memory was imprecise. Feedforward inhibition growth and memory precision were both rescued by re-expression of Add2 specifically in hippocampal mossy fibres. These results establish a causal relationship between learning-related increases in the numbers of defined synapses and the precision of learning and memory in the adult. The results further relate plasticity and feedforward inhibition growth at hippocampal mossy fibres to the precision of hippocampus-dependent memories.     

The endogenous cannabinoid system controls extinction of aversive memories

Acquisition and storage of aversive memories is one of the basic principles of central nervous systems throughout the animal kingdom. In the absence of reinforcement, the resulting behavioural response will gradually diminish to be finally extinct. Despite the importance of extinction, its cellular mechanisms are largely unknown. The cannabinoid receptor 1 (CB1) and endocannabinoids are present in memory-related brain areas and modulate memory. Here we show that the endogenous cannabinoid system has a central function in extinction of aversive memories. CB1-deficient mice showed strongly impaired short-term and long-term extinction in auditory fear-conditioning tests, with unaffected memory acquisition and consolidation. Treatment of wild-type mice with the CB1 antagonist SR141716A mimicked the phenotype of CB1-deficient mice, revealing that CB1 is required at the moment of memory extinction. Consistently, tone presentation during extinction trials resulted in elevated levels of endocannabinoids in the basolateral amygdala complex, a region known to control extinction of aversive memories. In the basolateral amygdala, endocannabinoids and CB1 were crucially involved in long-term depression of GABA (gamma-aminobutyric acid)-mediated inhibitory currents. We propose that endocannabinoids facilitate extinction of aversive memories through their selective inhibitory effects on local inhibitory networks in the amygdala.     

What are the memory sources of dreaming?

Investigators since Freud have appreciated that memories of the people, places, activities and emotions of daily life are reflected in dreams but are typically so fragmented that their predictability is nil. The mechanisms that translate such memories into dream images remain largely unknown. New research targeting relationships between dreaming, memory and the hippocampus is producing a new theory to explain how, why and when we dream of waking life events.     

《五号屠场》的创伤艺术与叙事疗伤

当今世界创伤依旧是时代烙印。美国杰出作家库尔特·冯内古特以战时经历为题材,创作了创伤小说《五号屠场》,以唤起人们对遭受战争创伤群体的关注。从创伤艺术的视角出发,解析冯内古特如何用叙事这一方式来消除创伤性记忆,以期为读者阅读本小说提供新的解读视角。     

记忆巩固效力研究述评

睡眠的记忆巩固在多大程度上取决于学习材料的类型、学习与提取测验的类型以及睡眠的不同特征？弱编码联系、外显编码的记忆相对于强编码联系、内隐编码的记忆提高得更多;慢波睡眠巩固陈述性记忆而快速眼动睡眠巩固程序性和情绪性记忆;陈述性记忆的提高来自相当短的睡眠时间,程序性记忆的提高似乎更多地取决于学习后当天的睡眠时间长度。     

Recovery of learning and memory is associated with chromatin remodelling

Neurodegenerative diseases of the central nervous system are often associated with impaired learning and memory, eventually leading to dementia. An important aspect in pre-clinical research is the exploration of strategies to re-establish learning ability and access to long-term memories. By using a mouse model that allows temporally and spatially restricted induction of neuronal loss, we show here that environmental enrichment reinstated learning behaviour and re-established access to long-term memories after significant brain atrophy and neuronal loss had already occurred. Environmental enrichment correlated with chromatin modifications (increased histone-tail acetylation). Moreover, increased histone acetylation by inhibitors of histone deacetylases induced sprouting of dendrites, an increased number of synapses, and reinstated learning behaviour and access to long-term memories. These data suggest that inhibition of histone deacetylases might be a suitable therapeutic avenue for neurodegenerative diseases associated with learning and memory impairment, and raises the possibility of recovery of long-term memories in patients with dementia.     

Sleep-dependent memory consolidation

The concept of 'sleeping on a problem' is familiar to most of us. But with myriad stages of sleep, forms of memory and processes of memory encoding and consolidation, sorting out how sleep contributes to memory has been anything but straightforward. Nevertheless, converging evidence, from the molecular to the phenomenological, leaves little doubt that offline memory reprocessing during sleep is an important component of how our memories are formed and ultimately shaped.