Life Sciences Commons^™

Apoaequorin Differentially Modulates Fear Conditioning In Adult And Aged Rats, Vanessa Ehlers

Theses and Dissertations

Normal aging is associated with a number of changes in behavioral and cellular function, and is often linked to increased susceptibility to cognitive impairment. The hippocampus has been widely implicated in learning and memory, and many forms of learning that are hippocampus-dependent (e.g. trace fear conditioning) are impaired in aged animals. A proposed contributor to aging-related cognitive impairment is aging-related calcium (Ca2+) dysregulation. This dysregulation is thought to result from changes in specific Ca2+-regulatory mechanisms, including abnormal Ca2+ ion channel activity or expression, as well as reduced Ca2+-binding protein (CaBP) expression, which is associated with cognitive and synaptic impairment. Previous …

Neural Plasticity Of Extinction: Relations With Anxiety And Extinction Retention, Emily Louise Belleau

Theses and Dissertations

ABSTRACT

NEURAL PLASTICITY OF EXTINCTION LEARNING: RELATIONS WITH ANXIETY AND EXTINCTION RETENTION

by

Emily L. Belleau

The University of Wisconsin-Milwaukee, 2016

Under the Supervision of Associate Professor Christine Larson

Anxiety is a significant public health problem characterized by substantial psychological, physical, and economic burden. A key feature of anxiety is the inability to regulate fear. Aberrant extinction of conditioned fear is one prominent model of the etiology of anxiety disorders. Previous studies have shown that the neural circuitry underlying anxiety pathology overlaps with that mediating fear extinction learning. Recently, more precise pathways supporting the expression (CMA-aMCC) and inhibition (BLA-vmPFC) of …

Changes In Resting-State Functional Connectivity Following Delay And Trace Fear Conditioning Acquisition And Extinction, Douglas Hank Schultz

Theses and Dissertations

Consolidation is the process of stabilizing a recently acquired memory into a more permanent or durable form. Several studies with laboratory animals have uncovered valuable information about the process of consolidation, but less is known about the process of consolidation in healthy humans. The current study examined the consolidation of emotional memories in different brain circuits in healthy humans using resting-state fMRI. We used the acquisition and extinction of two variations of Pavlovian fear conditioning, delay and trace, which rely on slightly different circuits to examine changes in functional connectivity related to a general fear learning process and also to …

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

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 …