Early and persistent dendritic hypertrophy in the basolateral amygdala following experimental diffuse traumatic brain injury

Ann N. Hoffman, Pooja R. Paode, Hazel G. May, J. Bryce Ortiz, Salma Kemmou, Jonathan Lifshitz, Cheryl Conrad, Theresa Currier Thomas

Research output: Contribution to journalArticle

11 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)213-219
Number of pages7
JournalJournal of Neurotrauma
Volume34
Issue number1
DOIs
StatePublished - Jan 1 2017

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Hypertrophy
Glial Fibrillary Acidic Protein
Wounds and Injuries
Brain
Post-Traumatic Stress Disorders
Amygdala
Percussion
Diffuse Brain Injury
Basolateral Nuclear Complex
Traumatic Brain Injury
Anxiety Disorders
Automatic Data Processing
Silver
Astrocytes
Psychiatry
Coloring Agents
Learning
Staining and Labeling
Neurons

Keywords

  • amygdala
  • comorbidity
  • plasticity
  • post-traumatic stress disorder
  • traumatic brain injury

ASJC Scopus subject areas

  • Clinical Neurology

Cite this

Hoffman, A. N., Paode, P. R., May, H. G., Ortiz, J. B., Kemmou, S., Lifshitz, J., ... Currier Thomas, T. (2017). Early and persistent dendritic hypertrophy in the basolateral amygdala following experimental diffuse traumatic brain injury. Journal of Neurotrauma, 34(1), 213-219. https://doi.org/10.1089/neu.2015.4339

Early and persistent dendritic hypertrophy in the basolateral amygdala following experimental diffuse traumatic brain injury. / Hoffman, Ann N.; Paode, Pooja R.; May, Hazel G.; Ortiz, J. Bryce; Kemmou, Salma; Lifshitz, Jonathan; Conrad, Cheryl; Currier Thomas, Theresa.

In: Journal of Neurotrauma, Vol. 34, No. 1, 01.01.2017, p. 213-219.

Research output: Contribution to journalArticle

Hoffman, Ann N. ; Paode, Pooja R. ; May, Hazel G. ; Ortiz, J. Bryce ; Kemmou, Salma ; Lifshitz, Jonathan ; Conrad, Cheryl ; Currier Thomas, Theresa. / Early and persistent dendritic hypertrophy in the basolateral amygdala following experimental diffuse traumatic brain injury. In: Journal of Neurotrauma. 2017 ; Vol. 34, No. 1. pp. 213-219.
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