• Demetrio Sierra-Mercado, Lauren M McAllister, Christopher C H Lee, Mohammed R Milad, Emad N Eskandar, and Michael J Whalen.
• Neuroscience Center and Department of Pediatrics, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, United States; Department of Neurosurgery, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, United States; Department of Anatomy & Neurobiology, University of Puerto Rico School of Medicine, San Juan, Puerto Rico, 00936. Electronic address: demetrio.sierra@upr.edu.
• Brain Res. 2015 May 5; 1606: 133-41.

AbstractPost-traumatic stress disorder (PTSD) is characterized in part by impaired extinction of conditioned fear. Traumatic brain injury (TBI) is thought to be a risk factor for development of PTSD. We tested the hypothesis that controlled cortical impact (CCI) would impair extinction of fear learned by Pavlovian conditioning, in mice. To mimic the scenarios in which TBI occurs prior to or after exposure to an aversive event, severe CCI was delivered to the left parietal cortex at one of two time points: (1) Prior to fear conditioning, or (2) after conditioning. Delay auditory conditioning was achieved by pairing a tone with a foot shock in "context A". Extinction training involved the presentation of tones in a different context (context B) in the absence of foot shock. Test for extinction memory was achieved by presentation of additional tones alone in context B over the following two days. In pre- or post-injury paradigms, CCI did not influence fear learning and extinction. Furthermore, CCI did not affect locomotor activity or elevated plus maze testing. Our results demonstrate that, within the time frame studied, CCI does not impair the acquisition and expression of conditioned fear or extinction memory.Copyright © 2015 Elsevier B.V. All rights reserved.

29 keywords...

hide…