Research Applications for Striatech Products

Traumatic Brain Injury (TBI)

Publications on Traumatic Brain Injury (TBI)

Experimental Eye Research (Feb 01, 2024) Increasing the number and intensity of shock tube generated blast waves leads to earlier retinal ganglion cell dysfunction and regional cell death

Harper MM, Boehme NA, Dutca L, Navarro V

DOI: 10.1016/j.exer.2023.109754 >>

Featured image for “Increasing the number and intensity of shock tube generated blast waves leads to earlier retinal ganglion cell dysfunction and regional cell death”

This study investigated the effects of blast exposure on retinal ganglion cell (RGC) function and structure in mice. Researchers used a shock tube to deliver blast waves of varying intensities and frequencies. They found that higher blast intensities and multiple exposures led to earlier functional loss of RGCs, with the most severe condition (30 PSI x 3) causing regional RGC loss in the central retina. The study utilized various techniques to assess retinal health, including pattern electroretinogram (PERG) and optical coherence tomography (OCT). The OptoDrum was employed to measure the optomotor reflex (OMR), providing crucial data on visual function that contributed to the overall assessment of blast-induced retinal damage.

The purpose of this study was to examine the effect of a blast exposure generated from a shock tube on retinal ganglion cell (RGC) function and structure. Mice were exposed to one of three blast conditions using a shock tube; a single blast wave of 20 PSI, a single blast wave of 30 PSI, or three blast waves of 30 PSI given on three consecutive days with a one-day inter-blast interval. The structure and function of the retina were analyzed using the pattern electroretinogram (PERG), the optomotor reflex (OMR), and optical coherence tomography (OCT). The in vivo parameters were examined at baseline, and then again 1-week, 4-weeks, and 16-weeks following blast exposure. The number of surviving RGCs was quantified at the end of the study. Analysis of mice receiving a 20 PSI injury showed decreased PERG and OMR responses 16-weeks post blast, without evidence of changed retinal thickness or RGC death. Mice subjected to a 30 PSI injury showed decreased PERG responses 4 weeks and 16 weeks after injury, without changes in the retinal thickness or RGC density. Mice subjected to 30 PSI X 3 blast exposures had PERG deficits 1-week and 4-weeks post exposure. There was also significant change in retinal thickness 1-week and 16-weeks post blast exposure. Mice receiving 30 PSI X 3 blast injuries had regional loss of RGCs in the central retina, but not in the mid-peripheral or peripheral retina. Overall, this study has shown that increasing the number of blast exposures and the intensity leads to earlier functional loss of RGCs. We have also shown regional RGC loss only when using the highest blast intensity and number of blast injuries.

Related Products:

OptoDrum

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Applications:
09 CNS Trauma and Acute Injury: TBI, Optic Nerve Injury, Stroke
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Cell Death
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Retinal Ganglion Cell Dysfunction
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Traumatic Brain Injury (TBI)
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Experimental Eye Research (Oct 06, 2022) Immune responses in mice after blast-mediated traumatic brain injury TBI autonomously contribute to retinal ganglion cell dysfunction and death

Harper MM, Gramlich OW, Elwood BW, Boehme NA, Dutca LM, Kuehn MH

DOI: 10.1016/j.exer.2022.109272 >>

Blast injuries are common in modern warfare. They lead to immediate damage to the nervous system, but often develop into chronic disease with progressive deterioration, including in the visual system. It is proposed that neuroinflammatory processes underly this chronic phase. 4 weeks after injury, Harper et al transferred splenocytes of mice exposed to blast-mediated traumatic brain injury (bTBI) into naïve animals. Those naïve animals developed visual symptoms and experienced ganglion cell dysfunction similar to the blast-injured mice, suggesting that the immune system is indeed involved in the chronic phase of bTBI.

Purpose: The purpose of this study was to examine the role of the immune system and its influence on chronic retinal ganglion cell (RGC) dysfunction following blast-mediated traumatic brain injury (bTBI). Methods: C57BL/6J and B6.129S7-Rag1^tm1Mom/J (Rag^-/-) mice were exposed to one blast injury of 140 kPa. A separate cohort of C57BL/6J mice was exposed to sham-blast. Four weeks following bTBI mice were euthanized, and splenocytes were collected. Adoptive transfer (AT) of splenocytes into naïve C57BL/6J recipient mice was accomplished via tail vein injection. Three groups of mice were analyzed: those receiving AT of splenocytes from C57BL/6J mice exposed to blast (AT-TBI), those receiving AT of splenocytes from C57BL/6J mice exposed to sham (AT-Sham), and those receiving AT of splenocytes from Rag^-/- mice exposed to blast (AT-Rag^-/-). The visual function of recipient mice was analyzed with the pattern electroretinogram (PERG), and the optomotor response (OMR). The structure of the retina was evaluated using optical coherence tomography (OCT), and histologically using BRN3A-antibody staining. Results: Analysis of the PERG showed a decreased amplitude two months post-AT that persisted for the duration of the study in AT-TBI mice. We also observed a significant decrease in the retinal thickness of AT-TBI mice two months post-AT compared to sham, but not at four or six months post-AT. The OMR response was significantly decreased in AT-TBI mice 5- and 6-months post-AT. BRN3A staining showed a loss of RGCs in AT-TBI and AT-Rag^-/- mice. Conclusion: These results suggest that the immune system contributes to chronic RGC dysfunction following bTBI.