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Permanent link (DOI): https://doi.org/10.7939/R30863J1S

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Mediation of memory permanence: Neural activity versus protein synthesis Open Access

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Other title
Subject/Keyword
memory
protein synthesis
neural activity
Type of item
Thesis
Degree grantor
University of Alberta
Author or creator
Rimstad, Lisa A
Supervisor and department
Dickson, Clayton T. (Psychology)
Examining committee member and department
Kerr, Bradley (Medical Sciences-Anaesthesia and Pain Medicine)
Bolduc, Francois (Medical Sciences-Medical Genetics)
Ali, Declan (Physiology)
Department
Centre for Neuroscience
Specialization

Date accepted
2017-01-13T11:28:30Z
Graduation date
2017-06:Spring 2017
Degree
Master of Science
Degree level
Master's
Abstract
Memory research has progressed substantially in the recent past, yet the mechanisms responsible for memory formation and permanence are still not well established. Much of this research has been focused on the events that occur at the level of the cell, leading to many molecular theories about the process of learning and memory. Currently, the prevailing explanation for how long-term memories are established is the de novo protein synthesis hypothesis, which suggests that new proteins are required to stabilize a memory trace. This hypothesis is primarily supported by studies that demonstrated memory deficits in experimental animals treated with protein synthesis inhibitors (PSIs). Recent work, however, has shown that PSIs suppress spontaneous and evoked neural activity in the hippocampus, suggesting that the memory impairments caused by protein synthesis inhibition may actually be attributed to altered neural activity. If PSIs, such as anisomycin (ANI), function by silencing neural activity, then their effects on behaviour would be functionally similar to that of drugs which temporarily inactivate neural tissue. In this thesis I tested the effect of pre-training microinfusions of ANI, tetrodotoxin (TTX), muscimol (MUSC), or a vehicle (PBS) on unconditioned fear, as well as on short- and long-term memory. TTX and MUSC are commonly used to temporarily inactivate neural tissue by blocking sodium channels and by binding to GABAA receptors, respectively, and act as positive controls for the neural suppressive effects of ANI. I injected one of these four solutions bilaterally into the basolateral amygdala of rats prior to an unconditioned fear test and training on an auditory fear conditioning task. All animals were then tested for short- and long-term memory of the fear conditioning task as measured by active freezing. The results of this study indicate that infusions of ANI, TTX, and MUSC result in significantly less freezing to the auditory cue at both short-term (2 hour) and long-term (24 hour) time points as compared to the PBS group. This indicates that ANI can disrupt both short- and long-term memory to the same extent as other neural inactivation techniques. These results challenge the de novo protein synthesis hypothesis of memory and suggest it must be carefully reexamined.
Language
English
DOI
doi:10.7939/R30863J1S
Rights
This thesis is made available by the University of Alberta Libraries with permission of the copyright owner solely for the purpose of private, scholarly or scientific research. This thesis, or any portion thereof, may not otherwise be copied or reproduced without the written consent of the copyright owner, except to the extent permitted by Canadian copyright law.
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