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PARK, JUNCHOL (2017) A NEURAL BASIS FOR THE BEHAVIORAL EFFECTS OF ANXIETY. Doctoral Dissertation, University of Pittsburgh. (Unpublished)

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Anxiety represents a state of high arousal and negative valence that leads to enhanced vigilance in the absence of concrete and immediate threat. Anxiety has profound impacts on ongoing behaviors. It can be an adaptive reaction to stressful or unpredictable life events, but excessive and persistent anxiety produces adverse cognitive effects that disrupt ongoing behavior and contribute to the clinical manifestation of anxiety disorders. Numerous studies have associated anxiety with deficits in cognitive control of behavior, and with perseverative behavioral tendencies. In addition, the adverse impact of anxiety is characterized in part by deficits in reward-related behavioral domains such as anhedonia and aberrant reward-associated perception.
This dissertation study focuses on the neural basis of the behavioral impacts of anxiety. The neural circuit, comprising the prefrontal cortex (PFC) and the ventral tegmental area (VTA), is thought to be critically involved in anxiety-induced behavioral disruptions. Numerous neurophysiological and neurochemical studies suggest that the mesoprefrontal circuit preferentially responds to aversive stimuli, stressors, and resultant anxiety. However, it is largely unknown how VTA and mPFC individual neurons and neuronal ensembles represent cognitive, motivational, and emotional behavioral changes in anxiety. To address this, we studied animals engaged in well-characterized motivated and cognitive behavioral tasks in the absence or presence of varying degrees of an anxiogenic perturbation. By electrophysiologically recording the activity of VTA and mPFC single neurons and local field potential (LFP) signals from the task-performing animals, we demonstrate that anxiety-related behavioral alterations can be attributed to specific changes in the activity of VTA and mPFC neurons and neuronal populations. Collectively, our neurophysiological findings suggest that anxiety “hijacks” the VTA-mPFC neural circuit by profoundly modulating the spontaneous and task-related neural activity at the individual neuron-, neural population-, and neural circuit levels. Anxiety-induced neural changes in the VTA-mPFC circuit were systematically associated with anxiety-like changes in motivated and cognitive behaviors, even on a single-trial basis, providing insights that could contribute to therapeutic interventions for the behavioral symptoms of anxiety disorders.


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Item Type: University of Pittsburgh ETD
Status: Unpublished
CreatorsEmailPitt UsernameORCID
PARK, JUNCHOLjup36@pitt.edujup36jup36
ETD Committee:
TitleMemberEmail AddressPitt UsernameORCID
Committee ChairMoghaddam,
Committee MemberSesack,
Committee MemberCohen,
Committee MemberAnne-Marie,
Committee MemberRobert,
Committee MemberUchida,
Date: 30 June 2017
Date Type: Publication
Defense Date: 12 December 2016
Approval Date: 30 June 2017
Submission Date: 19 December 2016
Access Restriction: 2 year -- Restrict access to University of Pittsburgh for a period of 2 years.
Number of Pages: 197
Institution: University of Pittsburgh
Schools and Programs: Dietrich School of Arts and Sciences > Neuroscience
Degree: PhD - Doctor of Philosophy
Thesis Type: Doctoral Dissertation
Refereed: Yes
Uncontrolled Keywords: Anxiety, Prefrontal cortex, Ventral tegmental area, Cognition, Motivation, Neurophysiology
Date Deposited: 30 Jun 2017 20:01
Last Modified: 30 Jun 2019 05:15


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