Using c-Jun to identify fear extinction learning-specific patterns of neural activity that are affected by single prolonged stress.

Autor: Knox D; Department of Psychological and Brain Sciences, University of Delaware, Newark, DE 19716, United States. Electronic address: dknox@psych.udel.edu., Stanfield BR; Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, NJ 07102, United States., Staib JM; Department of Neuroscience, University of Pennsylvania, Philadelphia, PA 19104, United States., David NP; School of Public Policy and Administration, University of Delaware, Newark, DE 19716, United States., DePietro T; Department of Psychological and Brain Sciences, University of Delaware, Newark, DE 19716, United States., Chamness M; Department of Psychological and Brain Sciences, University of Delaware, Newark, DE 19716, United States., Schneider EK; Department of Psychological and Brain Sciences, University of Delaware, Newark, DE 19716, United States., Keller SM; Department of Psychological and Brain Sciences, University of Delaware, Newark, DE 19716, United States., Lawless C; Department of Psychological and Brain Sciences, University of Delaware, Newark, DE 19716, United States.
Jazyk: angličtina
Zdroj: Behavioural brain research [Behav Brain Res] 2018 Apr 02; Vol. 341, pp. 189-197. Date of Electronic Publication: 2017 Dec 29.
DOI: 10.1016/j.bbr.2017.12.037
Abstrakt: Neural circuits via which stress leads to disruptions in fear extinction is often explored in animal stress models. Using the single prolonged stress (SPS) model of post traumatic stress disorder and the immediate early gene (IEG) c-Fos as a measure of neural activity, we previously identified patterns of neural activity through which SPS disrupts extinction retention. However, none of these stress effects were specific to fear or extinction learning and memory. C-Jun is another IEG that is sometimes regulated in a different manner to c-Fos and could be used to identify emotional learning/memory specific patterns of neural activity that are sensitive to SPS. Animals were either fear conditioned (CS-fear) or presented with CSs only (CS-only) then subjected to extinction training and testing. C-Jun was then assayed within neural substrates critical for extinction memory. Inhibited c-Jun levels in the hippocampus (Hipp) and enhanced functional connectivity between the ventromedial prefrontal cortex (vmPFC) and basolateral amygdala (BLA) during extinction training was disrupted by SPS in the CS-fear group only. As a result, these effects were specific to emotional learning/memory. SPS also disrupted inhibited Hipp c-Jun levels, enhanced BLA c-Jun levels, and altered functional connectivity among the vmPFC, BLA, and Hipp during extinction testing in SPS rats in the CS-fear and CS-only groups. As a result, these effects were not specific to emotional learning/memory. Our findings suggest that SPS disrupts neural activity specific to extinction memory, but may also disrupt the retention of fear extinction by mechanisms that do not involve emotional learning/memory.
(Copyright © 2017 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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