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dc.contributor.authorSharma, Avirale
dc.contributor.authorSura, Suvarsha
dc.contributor.authorChaudhary, Rafay
dc.contributor.authorFatima, Sumbul
dc.date.accessioned2018-02-12T17:19:35Z
dc.date.available2018-02-12T17:19:35Z
dc.date.issued2018-02-12
dc.date.submitted26-JAN-2018 03:09PM
dc.identifier.urihttp://hdl.handle.net/10675.2/621739
dc.descriptionPresentation given at the 19th Annual Phi Kappa Phi Student Research and Fine Arts Conferenceen
dc.description.abstractBackground: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.
dc.subjectS100A1en
dc.subjectPediatric traumatic brain injury (PedTBI)en
dc.subjectDepressionen
dc.titleS100A1 IS ESSENTIAL FOR PEDIATRIC TRAUMATIC BRAIN INJURY (PEDTBI) INDUCED DEPRESSIVE BEHAVIORen
dc.typePoster Presentationen
dc.contributor.departmentCollege of Science and Mathematicsen
dc.contributor.departmentDepartment of Medical Laboratory, Imaging and Radiologic Sciencesen
cr.funding.sourceAugusta University startup funden
dc.contributor.sponsorPandya, Chirayuen
dc.contributor.sponsorDepartment of Medical Laboratory, Imaging and Radiologic Sciencesen
dc.contributor.sponsorHoda, Md Nasrulen
dc.contributor.affiliationAugusta Universityen
dc.contributor.affiliationLakeside High School, Evans, GAen
html.description.abstractBackground: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.


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