Citation

Hoffman AN, Lam J, Hovda DA, Giza CC, Fanselow MS. Sci. Rep. 2019; 9(1): e13841.

Affiliation

Staglin Center for Brain and Behavioral Health, Life Sciences, UCLA, Los Angeles, USA.

Copyright

(Copyright © 2019, Nature Publishing Group)

DOI

10.1038/s41598-019-50312-y

PMID

31554865

Abstract

Traumatic brain injury (TBI) is one of the most common injuries to military personnel, a population often exposed to stressful stimuli and emotional trauma. Changes in sensory processing after TBI might contribute to TBI-post traumatic stress disorder (PTSD) comorbidity. Combining an animal model of TBI with an animal model of emotional trauma, we reveal an interaction between auditory sensitivity after TBI and fear conditioning where 75 dB white noise alone evokes a phonophobia-like phenotype and when paired with footshocks, fear is robustly enhanced. TBI reduced neuronal activity in the hippocampus but increased activity in the ipsilateral lateral amygdala (LA) when exposed to white noise. The white noise effect in LA was driven by increased activity in neurons projecting from ipsilateral auditory thalamus (medial geniculate nucleus). These data suggest that altered sensory processing within subcortical sensory-emotional circuitry after TBI results in neutral stimuli adopting aversive properties with a corresponding impact on facilitating trauma memories and may contribute to TBI-PTSD comorbidity.

Language: en