Persisting Alterations in Amygdala Neuronal Dendrites After Diffuse Traumatic Brain Injury

There is an emerging link between traumatic brain injury (TBI) and post traumatic stress disorder (PTSD), and the increasing numbers of veterans with TBI has created interest in their comorbidities. The amygdala is known to be involved in processing emotional and stressful stimuli, and is implicated in PTSD. Moreover, chronically stressed rats display dendritic restructuring in the amygdala, which persists for at least 21 days after the stressor manipulation has terminated. Even a single stressor manipulation can produce long-lasting changes in amygdala dendritic architecture. The amygdala has been largely understudied in TBI research and reorganization in this structure may serve as a nidus for TBI-induced PTSD affective symptoms and a future target for treatment. The purpose of this study was to quantify temporal changes in dendritic complexity within the basolateral amygdale (BLA) following a single diffuse TBI using a midline fluid percussion injury model. Adult male rats were subjected to a single moderate severity midline fluid percussion injury (FPI), or sham surgery (SHAM). At post injury days (PID) 1, 7 and 28, sham and brain-injured rats were euthanized and brains were collected and processed for Golgi stain analysis (200μm sections; FD Neurotechnologies Rapid GolgiStain^TM kit) to quantify dendritic complexity of individual BLA neurons. Fully stained, untruncated, and isolated pyramidal and stellate neurons were identified and reconstructed using a camera lucida microscope. The total number of branch points and overall dendritic length were quantified using the Sholl analysis at 20 µm increments. Compared to sham, brain-injured rats at all PID investigated (1, 7, 28) expressed enhanced dendritic complexity of BLA neurons. In pyramidal neurons, there was a significant interaction of group (SHAM, FPI-D1, FPI-D7, FPI-D28) across distance from soma. In stellate neurons, there was a significant interaction of group (SHAM, FPI-D1, FPI-D7, FPI-D28) across distance from soma, as well as a main effect for group (SHAM ≠ FPI-D1, FPI-D7, FPI-D28). These data suggest chronic enhancement of dendritic complexity within the BLA after a single TBI. Increased dendritic complexity would necessarily alter information processing into and through the extended amygdala, which may generate a long-term risk factor to, or precipitate the development of, PTSD after brain trauma. The amygdala remains a central focus for the continued analysis in the wake of TBI, as enduring structural alterations within the BLA after TBI may underlie the TBI-PTSD comorbidity.