Transcranial photobiomodulation prevents PTSD-like comorbidities in rats experiencing underwater trauma

• Published in: Translational psychiatry 2021-05, Vol.11 (1), p.270-270, Article 270
• Main Authors: Li, Yong, Dong, Yan, Yang, Luodan, Tucker, Lorelei, Yang, Baocheng, Zong, Xuemei, Hamblin, Michael R., Zhang, Quanguang
• Format: Article
• Language: English
• Subjects: 13/1; 14/34; 38; 38/77; 38/90; 631/378/340; 692/699/476/1414; 82; 82/29; 82/58; 82/80; Animals; Anxiety; Behavioral Sciences; Biological Psychology; Comorbidity; Fear; Light therapy; Medicine; Medicine & Public Health; Memory; Neurosciences; Pharmacotherapy; Post traumatic stress disorder; Psychiatry; Rats; Stress Disorders, Post-Traumatic
• ISSN: 2158-3188; 2158-3188
• DOI: 10.1038/s41398-021-01389-5

Maladaptive fear memory processing after a traumatic event is a major contributor to the development of the comorbidities related to posttraumatic stress disorder (PTSD). An intervention to normalize this process could be a first-line treatment to prevent PTSD development. However, little progress has been made in identifying interventions that can prevent trauma survivors from developing PTSD. A treatment that could help trauma survivors cope with traumatic memories and decrease the prevalence of PTSD is thus in high demand. This study was designed to investigate the potential beneficial effects of early photobiomodulation (PBM) interventions to prevent PTSD-like comorbidities in animals. PTSD-like comorbidities in rats were induced by an underwater trauma (UWT) procedure, followed by multiple swimming sessions on later days for memory recall. Immediately after UWT and swimming, rats were restrained with or without PBM treatment (808 nm, 25 mW/cm 2 , 3 J/day). PTSD-like commodities, such as anxiety-like behavior, depression-like behavior, and cognitive dysfunction, were reproduced in UWT-rats. These comorbidities, however, could be prevented by early PBM interventions. By measuring the expression of immediate early genes (IEGs) as neuronal activity markers, we found that PBM treatment differentially regulated Arc and c-fos expression in the hippocampus and amygdala, two PTSD-related brain regions. Additionally, PBM boosted ATP production and regulated protein expression in the hippocampus following stress. Our results demonstrate that PBM can modulate brain activity in response to traumatic and stressful events and that early PBM intervention can prevent the occurrence of PTSD-like comorbidities in rats.