scholarly journals A Late-Phase, Long-Term Memory Trace Forms in the   Neurons of Drosophila Mushroom Bodies after Olfactory Classical Conditioning

2010 ◽  
Vol 30 (49) ◽  
pp. 16699-16708 ◽  
Author(s):  
D.-B. G. Akalal ◽  
D. Yu ◽  
R. L. Davis
2010 ◽  
Vol 30 (18) ◽  
pp. 6461-6465 ◽  
Author(s):  
B. Hourcade ◽  
T. S. Muenz ◽  
J. C. Sandoz ◽  
W. Rossler ◽  
J. M. Devaud

Neuron ◽  
1999 ◽  
Vol 23 (4) ◽  
pp. 787-798 ◽  
Author(s):  
Scott T Wong ◽  
Jaime Athos ◽  
Xavier A Figueroa ◽  
Victor V Pineda ◽  
Michele L Schaefer ◽  
...  

1984 ◽  
Vol 55 (2) ◽  
pp. 363-370 ◽  
Author(s):  
Umur Talasli

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.


2020 ◽  
Vol 43 (1) ◽  
pp. 297-314 ◽  
Author(s):  
Josué Haubrich ◽  
Matteo Bernabo ◽  
Andrew G. Baker ◽  
Karim Nader

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.


Author(s):  
James S.H. Wong ◽  
Catharine H. Rankin

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.


1969 ◽  
Vol 2 (2) ◽  
pp. 135-173 ◽  
Author(s):  
Richard B. Roberts ◽  
Louis B. Flexner

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.


2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Yukinori Hirano ◽  
Kunio Ihara ◽  
Tomoko Masuda ◽  
Takuya Yamamoto ◽  
Ikuko Iwata ◽  
...  

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