Early and Persistent Dendritic Hypertrophy in the Basolateral Amygdala following Experimental Diffuse Traumatic Brain Injury.
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.
1 Department of Psychology, Arizona State University , Tempe, Arizona.|5 Department of Psychology, UCLA , Los Angeles, California.|6 Brain Injury Research Center, Department of Neurosurgery, David Geffen School of Medicine at UCLA , Los Angeles, California.
Ann N
AN
Hoffman
1 Department of Psychology, Arizona State University , Tempe, Arizona.
Pooja R
PR
Paode
2 Department of Child Health, University of Arizona College of Medicine-Phoenix , Phoenix, Arizona.|3 Barrow Neurological Institute at Phoenix Children's Hospital , Phoenix, Arizona.|7 Department of Biology and Biochemistry, University of Bath , Bath, United Kingdom .
Hazel G
HG
May
1 Department of Psychology, Arizona State University , Tempe, Arizona.
J Bryce
JB
Ortiz
1 Department of Psychology, Arizona State University , Tempe, Arizona.
Salma
S
Kemmou
1 Department of Psychology, Arizona State University , Tempe, Arizona.|2 Department of Child Health, University of Arizona College of Medicine-Phoenix , Phoenix, Arizona.|3 Barrow Neurological Institute at Phoenix Children's Hospital , Phoenix, Arizona.|4 Phoenix VA Healthcare System , Phoenix, Arizona.
Jonathan
J
Lifshitz
1 Department of Psychology, Arizona State University , Tempe, Arizona.
Cheryl D
CD
Conrad
2 Department of Child Health, University of Arizona College of Medicine-Phoenix , Phoenix, Arizona.|3 Barrow Neurological Institute at Phoenix Children's Hospital , Phoenix, Arizona.|4 Phoenix VA Healthcare System , Phoenix, Arizona.
Theresa
T
Currier Thomas
D000818:Animals; D066272:Basolateral Nuclear Complex / Q000473:pathology*; D000070625:Brain Injuries, Diffuse / Q000473:pathology*; D000070642:Brain Injuries, Traumatic / Q000150:complications / Q000473:pathology*; D003712:Dendrites / Q000473:pathology*; D006984:Hypertrophy; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
amygdala; comorbidity; plasticity; post-traumatic stress disorder; traumatic brain injury