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| Research article summary (published 26 Jan 2008): |
Auditory specific fear conditioning results in increased levels of synaptophysin in the basolateral amygdala.
Full Abstract
Auditory fear conditioning is one of the most well characterized models used in studies of learning and memory. In order to ensure the animals have been conditioned to fear the auditory stimulus, animals are generally tested for their response to this stimulus in a different context to that used for training. For this reason it is often unclear how much contextual fear conditioning the animals also acquire when they are trained. In this study, we have established a protocol for fear conditioning in mice which is explicit for auditory cues; mice trained using this protocol, show a very low fear response to contextual cues encountered during training. We have undertaken analysis to look for potential brain changes associated with this model by measuring levels of the synaptic vesicle protein, synaptophysin, in the basolateral nuclei of the amygdala following auditory fear conditioning. Our results show levels of synaptophysin were significantly higher in mice which learnt to associate the auditory stimulus with fear, in comparison to all non-learning control animals. These findings support the idea that synaptic plasticity associated with formation of fear conditioning to a single specific conditioned stimulus occurs within the basolateral nuclei of the amygdala. Furthermore, our results demonstrate the usefulness of this model in looking for changes in the brain specific for a defined learning event.
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Author information
Author/s: Nithianantharajah, Jess (J); Murphy, Mark (M);
Affiliation: Department of Anatomy and Cell Biology, University of Melbourne, Vic., Australia. jessn(-atsign-)florey.edu.au
Journal and publication information
Publication Type: Journal Article
Journal: Neurobiology of learning and memory (Neurobiol Learn Mem), published in United States. (Language: eng)
Reference: 2008-Jul; vol 90 (issue 1) : pp 36-43
Dates: Created 2008/06/10; Completed 2008/09/03;
PMID: 18226933, status: MEDLINE (last retrieval date: 11/6/2008)
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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