Molecular Mechanisms of Memory Storage inAplysia

2006 ◽  
Vol 210 (3) ◽  
pp. 174-191 ◽  
Author(s):  
Robert D. Hawkins ◽  
Eric R. Kandel ◽  
Craig H. Bailey
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.


2015 ◽  
Vol 26 (3) ◽  
Author(s):  
Zareen Amtul ◽  
Atta-ur-Rahman

AbstractDeciphering the cellular and molecular mechanisms of memory has been an important topic encompassing the learning and memory domain besides the neurodegenerative disorders. Synapses accumulate cognitive information from life-lasting alterations of their molecular and structural composition. Current memory storage models identify posttranslational modification imperative for short-term information storage and mRNA translation for long-term information storage. However, the precise account of these modifications has not been summarized at the individual synapse level. Therefore, herein we describe the spatiotemporal reorganization of synaptic plasticity at the dendritic spine level to elucidate the mechanism through which synaptic substructures are remodeled; though at the molecular level, such mechanisms are still quite unclear. It has thus been concluded that the existing mechanisms do not entirely elaborate memory storage processes. Further efforts are therefore encouraged to delineate the mechanism of neuronal connectivity at the chemical level as well, including inter- or intramolecular bonding patterns at the synaptic level, which may be a permissive and vital step of memory storage.


2018 ◽  
Vol 19 (10) ◽  
pp. 3033 ◽  
Author(s):  
James Robertson

The Neuron Doctrine, the cornerstone of research on normal and abnormal brain functions for over a century, has failed to discern the basis of complex cognitive functions. The location and mechanisms of memory storage and recall, consciousness, and learning, remain enigmatic. The purpose of this article is to critically review the Neuron Doctrine in light of empirical data over the past three decades. Similarly, the central role of the synapse and associated neural networks, as well as ancillary hypotheses, such as gamma synchrony and cortical minicolumns, are critically examined. It is concluded that each is fundamentally flawed and that, over the past three decades, the study of non-neuronal cells, particularly astrocytes, has shown that virtually all functions ascribed to neurons are largely the result of direct or indirect actions of glia continuously interacting with neurons and neural networks. Recognition of non-neural cells in higher brain functions is extremely important. The strict adherence of purely neurocentric ideas, deeply ingrained in the great majority of neuroscientists, remains a detriment to understanding normal and abnormal brain functions. By broadening brain information processing beyond neurons, progress in understanding higher level brain functions, as well as neurodegenerative and neurodevelopmental disorders, will progress beyond the impasse that has been evident for decades.


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 ◽  
...  

2005 ◽  
Vol 28 (1) ◽  
pp. 65-66
Author(s):  
Clive R. Bramham

Insights into the role of sleep in the molecular mechanisms of memory consolidation may come from studies of activity-dependent synaptic plasticity, such as long-term potentiation (LTP). This commentary posits a specific contribution of sleep to LTP stabilization, in which mRNA transported to dendrites during wakefulness is translated during sleep. Brain-derived neurotrophic factor may drive the translation of newly transported and resident mRNA.


Author(s):  
Kimberly Lackenby ◽  
Karl Peter Giese

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