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Citation |
Ratliff WA, Mervis RF, Citron BA, Schwartz B, Rubovitch V, Schreiber S, Pick CG. Exp. Neurol. 2019; 315: 9-14. |
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Affiliation |
Department of Anatomy and Anthropology, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel; Sagol School of Neuroscience, Tel Aviv University, Tel Aviv 69978, Israel; Dr. Miriam and Sheldon G. Adelson Chair, Center for the Biology of Addictive Diseases, Tel Aviv University, Tel Aviv 69978, Israel. |
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Copyright |
(Copyright © 2019, Elsevier Publishing) |
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DOI |
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PMID |
30711646 |
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Abstract |
Traumatic brain injury (TBI) continues to be a signature injury of our modern conflicts. Due in part to increased use of improvised explosive devices (IEDs), we have seen blast trauma make up a significant portion of TBIs sustained by deployed troops and civilians. In addition to the physical injury, TBI is also a common comorbidity with post-traumatic stress disorder (PTSD). Previous research suggests that PTSD is often associated with increased signaling within the amygdala, leading to feelings of fear and hyperarousal. In our study, we utilized a mouse model of mild blast-related TBI (bTBI) to investigate how TBI induces changes within the amygdala, which may provide favorable conditions for the development of PTSD. To do this, we performed Golgi staining on the stellate neurons of the basolateral amygdala and quantified dendritic amount, distribution, and complexity. We found increases in dendritic branching and in the density of dendritic spines in injured mice. Increases in spine density appears to be primarily due to increases in memory associated mushroom type dendritic spines. These changes observed in our bTBI model that are consistent with chronic stress models, suggesting an important connection between the physical changes induced by TBI and the neurological symptoms of PTSD. Language: en |
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Keywords |
Basolateral amygdala; Blast-related traumatic brain injury; Golgi stain; Post-traumatic stress disorder |