The Biochemical Basis of Long-Term Memory

1969 ◽  
Vol 2 (2) ◽  
pp. 135-173 ◽  
Author(s):  
Richard B. Roberts ◽  
Louis B. Flexner
Keyword(s):  
Learning And Memory ◽  
Memory Trace ◽  
Practical Interest ◽  
Long Term Memory ◽  
Daily Lives ◽  
Biochemical Basis ◽  
Term Memory ◽  
Actual Knowledge

Learning and memory are important elements of our daily lives, familiar to all through introspection. Yet the mechanisms underlying these processes are still for the most part unknown. Here are problems which combine a maximum of intrinsic and practical interest with a minimum of actual knowledge and understanding. Years of our lives are dedicated to the formation of certain long-term memories and behaviour patterns, yet we have only rudimentary notions of how such ‘schooling’ is best accomplished. There is no certainty in any aspect of the process. We are not sure whether relatively few cells or millions participate in a memory trace; whether these cells change as a whole, or whether the changes are limited to synaptic regions. In fact, we cannot be certain whether the changes are confined to the neurones or whether the glia also participate.

Proactive Inhibition as a Result of Activation

1984 ◽  
Vol 55 (2) ◽  
pp. 363-370 ◽  
Author(s):  
Umur Talasli
Keyword(s):  
Memory Trace ◽  
Proactive Inhibition ◽  
Long Term Memory ◽  
Term Memory ◽  
Initial Recall ◽  
Significant Attenuation ◽  
Presence And Absence

A novel encoding hypothesis that explains proactive inhibition in the Brown-Peterson paradigm was developed and tested in three experiments. This hypothesis argues that initial recall on each trial activates a pool of associates and the encoding of the next trial occurs during such activation. The encoding is facilitated and leaves a weak long-term memory trace. Build-up and release of inhibition, as well as a number of other typical results, are parsimoniously accounted for by such a mechanism. In support of the hypothesis, Exps. 1 and 2 demonstrated significant accentuation of proactive inhibition with increased activation both in the presence and absence of inter-trial category relationship. Exp. 3 showed significant attenuation of proactive inhibition as activation decayed. Increase in latency of recall with increased activation was also noted.

Impairments to Consolidation, Reconsolidation, and Long-Term Memory Maintenance Lead to Memory Erasure

2020 ◽  
Vol 43 (1) ◽  
pp. 297-314 ◽  
Author(s):  
Josué Haubrich ◽  
Matteo Bernabo ◽  
Andrew G. Baker ◽  
Karim Nader
Keyword(s):  
Memory Trace ◽  
Direct Approach ◽  
Long Term Memory ◽  
Retrieval Failure ◽  
Term Memory ◽  
The Brain

An enduring problem in neuroscience is determining whether cases of amnesia result from eradication of the memory trace (storage impairment) or if the trace is present but inaccessible (retrieval impairment). The most direct approach to resolving this question is to quantify changes in the brain mechanisms of long-term memory (BM-LTM). This approach argues that if the amnesia is due to a retrieval failure, BM-LTM should remain at levels comparable to trained, unimpaired animals. Conversely, if memories are erased, BM-LTM should be reduced to resemble untrained levels. Here we review the use of BM-LTM in a number of studies that induced amnesia by targeting memory maintenance or reconsolidation. The literature strongly suggests that such amnesia is due to storage rather than retrieval impairments. We also describe the shortcomings of the purely behavioral protocol that purports to show recovery from amnesia as a method of understanding the nature of amnesia.

scholarly journals Effects of Pramipexole on Learning and Memory Processes in Naïve and Haloperidol-challenged Rats in Active Avoidance Test

Folia Medica ◽  
2019 ◽  
Vol 61 (2) ◽  
pp. 258-265 ◽  
Author(s):  
Anita S. Mihaylova ◽  
Ilia D. Kostadinov ◽  
Nina D. Doncheva ◽  
Hristina I. Zlatanova ◽  
Delian P. Delev
Keyword(s):  
Learning And Memory ◽  
Active Avoidance ◽  
Memory Test ◽  
Long Term Memory ◽  
Motor Symptoms ◽  
Term Memory ◽  
Avoidance Test ◽  
Male Wistar Rats ◽  
Active Avoidance Test

Abstract Background: Parkinson’s disease (PD) is the second most common neurode-generative disease, usually detected by its motor symptoms. The non-motor symptoms, including cognitive deficits, have been of great interest to researchers in the last few decades. Aim: To assess the effect of pramipexole on learning and memory in naïve and haloperidol-challenged rats. Materials and methods: Male Wistar rats divided into 9 groups (n=8): naïve - saline, pramipexole 0.5; 1 and 3 mg/kg bw; Haloperidol groups - saline, haloperidol, haloperidol + pramipexole 0.5; 1 and 3 mg/kg bw. Two-way active avoidance test (TWAA) and activity cage were performed. The studied parameters were: number of conditioned and unconditioned responses, vertical and horizontal movements. Statistical analysis was done using SPSS 19. Results: The naïve experimental groups significantly increased the number of conditioned responses during the tests for short- and long-term memory, compared with the saline groups (p<0.05). During the short-memory test only the animals with the lowest dose of PMX significantly increased the number of unconditioned responses whereas during the long-term memory test all experimental groups increased the number of escapes in comparison with the saline groups (p<0.05). Challenge dose of haloperidol attenuates learning and memory in pramipexol treated rats. Only the highest dose of pramipexol showed significant increase in conditioned and unconditioned responses compared with the haloperidol group (p<0.05). Conclusion: Pramipexole improves learning and memory in naïve rats by enhancing dopaminergic neurotransmission. This is probably not the only mechanism involved. This is confirmed by the decrease in learning and memory ability in rats with haloperidol-challenge.

scholarly journals Endophilin A1 drives acute structural plasticity of dendritic spines in response to Ca2+/calmodulin

2021 ◽  
Vol 220 (6) ◽  
Author(s):  
Yanrui Yang ◽  
Jiang Chen ◽  
Xue Chen ◽  
Di Li ◽  
Jianfeng He ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Dendritic Spines ◽  
Actin Polymerization ◽  
Structural Plasticity ◽  
Long Term Potentiation ◽  
Membrane Dynamics ◽  
Long Term Memory ◽  
Term Memory ◽  
Term Potentiation

Induction of long-term potentiation (LTP) in excitatory neurons triggers a large transient increase in the volume of dendritic spines followed by decays to sustained size expansion, a process termed structural LTP (sLTP) that contributes to the cellular basis of learning and memory. Although mechanisms regulating the early and sustained phases of sLTP have been studied intensively, how the acute spine enlargement immediately after LTP stimulation is achieved remains elusive. Here, we report that endophilin A1 orchestrates membrane dynamics with actin polymerization to initiate spine enlargement in NMDAR-mediated LTP. Upon LTP induction, Ca2+/calmodulin enhances binding of endophilin A1 to both membrane and p140Cap, a cytoskeletal regulator. Consequently, endophilin A1 rapidly localizes to the plasma membrane and recruits p140Cap to promote local actin polymerization, leading to spine head expansion. Moreover, its molecular functions in activity-induced rapid spine growth are required for LTP and long-term memory. Thus, endophilin A1 serves as a calmodulin effector to drive acute structural plasticity necessary for learning and memory.

Caenorhabditis elegans Learning and Memory

2019 ◽  
Author(s):  
James S.H. Wong ◽  
Catharine H. Rankin
Keyword(s):  
Carbon Dioxide ◽  
Caenorhabditis Elegans ◽  
Classical Conditioning ◽  
Learning And Memory ◽  
Long Term Memory ◽  
Context Conditioning ◽  
Term Memory ◽  
C Elegans

The nematode, Caenorhabditis elegans (C. elegans), is an organism useful for the study of learning and memory at the molecular, cellular, neural circuitry, and behavioral levels. Its genetic tractability, transparency, connectome, and accessibility for in vivo cellular and molecular analyses are a few of the characteristics that make the organism such a powerful system for investigating mechanisms of learning and memory. It is able to learn and remember across many sensory modalities, including mechanosensation, chemosensation, thermosensation, oxygen sensing, and carbon dioxide sensing. C. elegans habituates to mechanosensory stimuli, and shows short-, intermediate-, and long-term memory, and context conditioning for mechanosensory habituation. The organism also displays chemotaxis to various chemicals, such as diacetyl and sodium chloride. This behavior is associated with several forms of learning, including state-dependent learning, classical conditioning, and aversive learning. C. elegans also shows thermotactic learning in which it learns to associate a particular temperature with the presence or absence of food. In addition, both oxygen preference and carbon dioxide avoidance in C. elegans can be altered by experience, indicating that they have memory for the oxygen or carbon dioxide environment they were reared in. Many of the genes found to underlie learning and memory in C. elegans are homologous to genes involved in learning and memory in mammals; two examples are crh-1, which is the C. elegans homolog of the cAMP response element-binding protein (CREB), and glr-1, which encodes an AMPA glutamate receptor subunit. Both of these genes are involved in long-term memory for tap habituation, context conditioning in tap habituation, and chemosensory classical conditioning. C. elegans offers the advantage of having a very small nervous system (302 neurons), thus it is possible to understand what these conserved genes are doing at the level of single identified neurons. As many mechanisms of learning and memory in C. elegans appear to be similar in more complex organisms including humans, research with C. elegans aids our ever-growing understanding of the fundamental mechanisms of learning and memory across the animal kingdom.

scholarly journals Cholesterol and Copper Affect Learning and Memory in the Rabbit

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Bernard G. Schreurs
Keyword(s):  
Learning And Memory ◽  
Rabbit Model ◽  
Dietary Cholesterol ◽  
Long Term Memory ◽  
Cholesterol Diet ◽  
Term Memory ◽  
Model Of Alzheimer’S Disease ◽  
Amyloid Accumulation

A rabbit model of Alzheimer’s disease based on feeding a cholesterol diet for eight weeks shows sixteen hallmarks of the disease including beta amyloid accumulation and learning and memory changes. Although we have shown that feeding 2% cholesterol and adding copper to the drinking water can retard learning, other studies have shown that feeding dietary cholesterol before learning can improve acquisition and feeding cholesterol after learning can degrade long-term memory. We explore the development of this model, the issues surrounding the role of copper, and the particular contributions of the late D. Larry Sparks.

scholarly journals Early Long-Term Memory Impairment and Changes in the Expression of Synaptic Plasticity-Associated Genes, in the McGill-R-Thy1-APP Rat Model of Alzheimer's-Like Brain Amyloidosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Martín Habif ◽  
Sonia Do Carmo ◽  
María Verónica Báez ◽  
Natalia Claudia Colettis ◽  
Magalí Cecilia Cercato ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Memory Deficits ◽  
Male Rats ◽  
Long Term Memory ◽  
Aβ Oligomers ◽  
Term Memory ◽  
Early Stages ◽  
Human Pathology

Accruing evidence supports the hypothesis that memory deficits in early Alzheimer Disease (AD) might be due to synaptic failure caused by accumulation of intracellular amyloid beta (Aβ) oligomers, then secreted to the extracellular media. Transgenic mouse AD models provide valuable information on AD pathology. However, the failure to translate these findings to humans calls for models that better recapitulate the human pathology. McGill-R-Thy1-APP transgenic (Tg) rat expresses the human amyloid precursor protein (APP751) with the Swedish and Indiana mutations (of familial AD), leading to an AD-like slow-progressing brain amyloid pathology. Therefore, it offers a unique opportunity to investigate learning and memory abilities at early stages of AD, when Aβ accumulation is restricted to the intracellular compartment, prior to plaque deposition. Our goal was to further investigate early deficits in memory, particularly long-term memory in McGill-R-Thy1-APP heterozygous (Tg+/–) rats. Short-term- and long-term habituation to an open field were preserved in 3-, 4-, and 6-month-old (Tg+/–). However, long-term memory of inhibitory avoidance to a foot-shock, novel object-recognition and social approaching behavior were seriously impaired in 4-month-old (Tg+/–) male rats, suggesting that they are unable to either consolidate and/or evoke such associative and discriminative memories with aversive, emotional and spatial components. The long-term memory deficits were accompanied by increased transcript levels of genes relevant to synaptic plasticity, learning and memory processing in the hippocampus, such as Grin2b, Dlg4, Camk2b, and Syn1. Our findings indicate that in addition to the previously well-documented deficits in learning and memory, McGill-R-Thy1-APP rats display particular long-term-memory deficits and deep social behavior alterations at pre-plaque early stages of the pathology. This highlights the importance of Aβ oligomers and emphasizes the validity of the model to study AD-like early processes, with potentially predictive value.

The pharmacology of long-term memory

1995 ◽  
Vol 3 (1) ◽  
pp. 35-48 ◽  
Author(s):  
Cesare Mondadori
Keyword(s):  
Memory Trace ◽  
Long Term Memory ◽  
Drug Induced ◽  
Term Memory ◽  
Memory Enhancing ◽  
Better Than

If information enters memory under the influence of a memory-enhancing substance, for about 16 hours thereafter the recollection of that information is no better than if it had been acquired without any treatment. Later tests of retention, however, performed one or more days, or even weeks, after the experience, show a drug-induced improvement of memory. Memory-enhancing compounds thus appear to facilitate the formation of the long-term memory trace. On the assumption that differences between treated and untreated animals emerge from that moment on when memory is based on the products of the processes modulated by the drugs, it can be postulated that long-term memory comes into play after about 16–20 hours.

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