Sharma, Avirale; Sura, Suvarsha; Chaudhary, Rafay; Fatima, Sumbul; College of Science and Mathematics; Department of Medical Laboratory, Imaging and Radiologic Sciences; Pandya, Chirayu; Department of Medical Laboratory, Imaging and Radiologic Sciences; Hoda, Md Nasrul; Augusta University; et al. (2018-02-12)
      Background:Majority of kids visit the emergency room due to a pediatric traumatic brain injury (PedTBI), which increases the risk of long-term prognosis. S100A1 is a small molecular weight calciumbinding protein, whichdifferentially regulates cell specific signaling. Hypothesis:We tested the hypothesis that increased neuronal-S100A1 expression after PedTBI exacerbates depression. Methods:Wild type (WT) or S100A1 KO mice (SKO; 3-weeks) were used for behavioral comparison. Male mice from both strains (3-weeks) were also subjected to a closed-head PedTBI, followed by neurobehavioral assessments and tissue biochemistry at 4-weeks. Statistical significance was determined at P<0.05. Results:Naïve SKO mice showed significant anti-depressive phenotype compared to the WT control, and were resistant to the post-PedTBI depression. In WT mice, PedTBI significantly increasedthe neuronal-S100A1 in the cortex compared to the control, which paralleled with the significant decrease in brain derived neurotrophic factor (BDNF) and synapsin I expressions, the key molecules in neural plasticity. Post-PedTBI loss in BDNF/Synapsin I and behavioral abnormalities due were reversed in the SKO mice. Conclusions:Our data identify neuronal-S100A1 as a possible link in the development of post-PedTBI depression. Further studies are warranted to establish the functional role of neuronal-S100A1in the development of depression after PedTBI.