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Social and Behavioral Sciences Commons

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Psychology

University of Wisconsin Milwaukee

2013

Fear Conditioning

Articles 1 - 2 of 2

Full-Text Articles in Social and Behavioral Sciences

The Role Of The Amygdala, Retrosplenial Cortex, And Medial Prefrontal Cortex In Trace Fear Extinction And Reconsolidation, Janine Lynn Kwapis Dec 2013

The Role Of The Amygdala, Retrosplenial Cortex, And Medial Prefrontal Cortex In Trace Fear Extinction And Reconsolidation, Janine Lynn Kwapis

Theses and Dissertations

A wealth of research has outlined the neural circuits responsible for the consolidation, reconsolidation, and extinction of standard "delay" fear conditioning, in which awareness is not required for learning. Far less is understood about the neural circuit supporting more complex, explicit associations. "Trace" fear conditioning is considered to be a rodent model of explicit fear because it relies on the cortex and hippocampus and requires explicit contingency awareness in humans for successful acquisition. In the current set of studies, we aimed to better characterize the neural circuit supporting the consolidation, reconsolidation, and extinction of trace fear in order to better …


The Role Of A Camkii/Pka-Protein Degradation-Glur2 Pathway In The Control Of Memory Updating Following Retrieval, Timothy Jarome Aug 2013

The Role Of A Camkii/Pka-Protein Degradation-Glur2 Pathway In The Control Of Memory Updating Following Retrieval, Timothy Jarome

Theses and Dissertations

Reconsolidation is thought to be a process whereby consolidated memories can be modified following retrieval. However, very little is known about the molecular mechanisms that regulate this reconsolidation process. In the present series of experiments we tested if memories "destabilize" or become labile following retrieval through a specific signaling pathway. We found that retrieval of a contextual fear memory differentially increased proteasome activity in the amygdala and hippocampus and resulted in unique changes in AMPA receptor subunit expression in these brain regions. These changes were dependent on CaMKII activity, which was required for increases in Rpt6-S120 phosphorylation, proteasome activity and …