Molecular mechanisms of memory formation

1991 ◽  
Vol 5 (2-4) ◽  
pp. 333-350 ◽  
Author(s):  
K. T. Ng ◽  
M. E. Gibbs ◽  
S. F. Crowe ◽  
G. L. Sedman ◽  
F. Hua ◽  
...  
1998 ◽  
Vol 6 (3) ◽  
pp. 41-52 ◽  
Author(s):  
Carmen Sandi

Adrenal steroid hormones modulate learning and memory processes by interacting with specific glucocorticoid receptors at different brain areas. In this article, certain components of the physiological response to stress elicited by learning situations are proposed to form an integral aspect of the neurobiological mechanism underlying memory formation. By reviewing the work carried out in different learning models in chicks (passive avoidance learning) and rats (spatial orientation in the Morris water maze and contextual fear conditioning), a role for brain corticosterone action through the glucocorticoid receptor type on the mechanisms of memory consolidation is hypothesized. Evidence is also presented to relate post-training corticosterone levels to the strength of memory storage. Finally, the possible molecular mechanisms that might mediate the influences of glucocorticoids in synaptic plasticity subserving long-term memory formation are considered, mainly by focusing on studies implicating a steroid action through (i) glutamatergic transmission and (ii) cell adhesion molecules.


2021 ◽  
Vol 22 (8) ◽  
pp. 4113
Author(s):  
Timothy J. Jarome ◽  
Janine L. Kwapis

Memory is vital to human functioning and controls future behavioral responses [...]


2021 ◽  
Vol 15 ◽  
Author(s):  
Camilla Roselli ◽  
Mani Ramaswami ◽  
Tamara Boto ◽  
Isaac Cervantes-Sandoval

Understanding the nature of the molecular mechanisms underlying memory formation, consolidation, and forgetting are some of the fascinating questions in modern neuroscience. The encoding, stabilization and elimination of memories, rely on the structural reorganization of synapses. These changes will enable the facilitation or depression of neural activity in response to the acquisition of new information. In other words, these changes affect the weight of specific nodes within a neural network. We know that these plastic reorganizations require de novo protein synthesis in the context of Long-term memory (LTM). This process depends on neural activity triggered by the learned experience. The use of model organisms like Drosophila melanogaster has been proven essential for advancing our knowledge in the field of neuroscience. Flies offer an optimal combination of a more straightforward nervous system, composed of a limited number of cells, and while still displaying complex behaviors. Studies in Drosophila neuroscience, which expanded over several decades, have been critical for understanding the cellular and molecular mechanisms leading to the synaptic and behavioral plasticity occurring in the context of learning and memory. This is possible thanks to sophisticated technical approaches that enable precise control of gene expression in the fruit fly as well as neural manipulation, like chemogenetics, thermogenetics, or optogenetics. The search for the identity of genes expressed as a result of memory acquisition has been an active interest since the origins of behavioral genetics. From screenings of more or less specific candidates to broader studies based on transcriptome analysis, our understanding of the genetic control behind LTM has expanded exponentially in the past years. Here we review recent literature regarding how the formation of memories induces a rapid, extensive and, in many cases, transient wave of transcriptional activity. After a consolidation period, transcriptome changes seem more stable and likely represent the synthesis of new proteins. The complexity of the circuitry involved in memory formation and consolidation is such that there are localized changes in neural activity, both regarding temporal dynamics and the nature of neurons and subcellular locations affected, hence inducing specific temporal and localized changes in protein expression. Different types of neurons are recruited at different times into memory traces. In LTM, the synthesis of new proteins is required in specific subsets of cells. This de novo translation can take place in the somatic cytoplasm and/or locally in distinct zones of compartmentalized synaptic activity, depending on the nature of the proteins and the plasticity-inducing processes that occur. We will also review recent advances in understanding how localized changes are confined to the relevant synapse. These recent studies have led to exciting discoveries regarding proteins that were not previously involved in learning and memory processes. This invaluable information will lead to future functional studies on the roles that hundreds of new molecular actors play in modulating neural activity.


2007 ◽  
Vol 8 (4) ◽  
pp. 262-275 ◽  
Author(s):  
Natalie C. Tronson ◽  
Jane R. Taylor

2009 ◽  
Vol 8 (3) ◽  
pp. 299-312 ◽  
Author(s):  
Andre Tanel ◽  
Simone G Fonseca ◽  
Bader Yassine-Diab ◽  
Rebeka Bordi ◽  
Joumana Zeidan ◽  
...  

2019 ◽  
Vol 31 (10) ◽  
pp. 1443-1454 ◽  
Author(s):  
Jessica K. Stanek ◽  
Kathryn C. Dickerson ◽  
Kimberly S. Chiew ◽  
Nathaniel J. Clement ◽  
R. Alison Adcock

Anticipating rewards has been shown to enhance memory formation. Although substantial evidence implicates dopamine in this behavioral effect, the precise mechanisms remain ambiguous. Because dopamine nuclei have been associated with two distinct physiological signatures of reward prediction, we hypothesized two dissociable effects on memory formation. These two signatures are a phasic dopamine response immediately following a reward cue that encodes its expected value and a sustained, ramping response that has been demonstrated during high reward uncertainty [Fiorillo, C. D., Tobler, P. N., & Schultz, W. Discrete coding of reward probability and uncertainty by dopamine neurons. Science, 299, 1898–1902, 2003]. Here, we show in humans that the impact of reward anticipation on memory for an event depends on its timing relative to these physiological signatures. By manipulating reward probability (100%, 50%, or 0%) and the timing of the event to be encoded (just after the reward cue versus just before expected reward outcome), we demonstrated the predicted double dissociation: Early during reward anticipation, memory formation was improved by increased expected reward value, whereas late during reward anticipation, memory formation was enhanced by reward uncertainty. Notably, although the memory benefits of high expected reward in the early interval were consolidation dependent, the memory benefits of high uncertainty in the later interval were not. These findings support the view that expected reward benefits memory consolidation via phasic dopamine release. The novel finding of a distinct memory enhancement, temporally consistent with sustained anticipatory dopamine release, points toward new mechanisms of memory modulation by reward now ripe for further investigation.


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