Early and Persistent Dendritic Hypertrophy in the Basolateral Amygdala following Experimental Diffuse Traumatic Brain Injury
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Final Accepted Manuscript
Author
Hoffman, Ann N.Paode, Pooja R.
May, Hazel G.
Ortiz, J. Bryce
Kemmou, Salma
Lifshitz, Jonathan
Conrad, Cheryl D.
Currier Thomas, Theresa
Affiliation
Department of Child Health, University of Arizona College of Medicine-PhoenixIssue Date
2017-01
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MARY ANN LIEBERT, INCCitation
Early and Persistent Dendritic Hypertrophy in the Basolateral Amygdala following Experimental Diffuse Traumatic Brain Injury 2017, 34 (1):213 Journal of NeurotraumaJournal
Journal of NeurotraumaRights
© Mary Ann Liebert, Inc.Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.Abstract
In the pathophysiology of traumatic brain injury (TBI), the amygdala remains understudied, despite involvement in processing emotional and stressful stimuli associated with anxiety disorders, such as post-traumatic stress disorder (PTSD). Because the basolateral amygdala (BLA) integrates inputs from sensory and other limbic structures coordinating emotional learning and memory, injury-induced changes in circuitry may contribute to psychiatric sequelae of TBI. This study quantified temporal changes in dendritic complexity of BLA neurons after experimental diffuse TBI, modeled by midline fluid percussion injury. At post-injury days (PIDs) 1, 7, and 28, brain tissue from sham and brain-injured adult, male rats was processed for Golgi, glial fibrillary acidic protein (GFAP), or silver stain and analyzed to quantify BLA dendritic branch intersections, activated astrocytes, and regional neuropathology, respectively. Compared to sham, brain-injured rats at all PIDs showed enhanced dendritic branch intersections in both pyramidal and stellate BLA neuronal types, as evidenced by Sholl analysis. GFAP staining in the BLA was significantly increased at PID1 and 7 in comparison to sham. However, the BLA was relatively spared from neuropathology, demonstrated by an absence of argyrophilic accumulation over time, in contrast to other brain regions. These data suggest an early and persistent enhancement of dendritic complexity within the BLA after a single diffuse TBI. Increased dendritic complexity would alter information processing into and through the amygdala, contributing to emotional symptoms post-TBI, including PTSD.Note
Online Ahead of Print: July 27, 2016; 12 month embargo.ISSN
0897-71511557-9042
Version
Final accepted manuscriptSponsors
Arizona Biomedical Research Commission through the Arizona Department of Health Services [ADHS14-00003606]; National Institute of Neurological Disorders and Stroke of the National Institutes of Health [R01 NS-065052]; Phoenix Children's HospitalAdditional Links
http://online.liebertpub.com/doi/10.1089/neu.2015.4339ae974a485f413a2113503eed53cd6c53
10.1089/neu.2015.4339