A novel mouse model of mild traumatic brain injury using laser-induced shock waves

Tomura, Satoshi; Seno, Soichiro; Kawauchi, Satoko; Miyazaki, Hiromi; Sato, Shunichi; Kobayashi, Yasushi; Saitoh, Daizoh

doi:10.1016/j.neulet.2020.134827

Cited by 9 publications

(7 citation statements)

References 31 publications

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“…Therefore, examination of neurogenesis indices 3 dpi may reveal changes that influence the subsequent emergence of 7 dpi DG hyperexcitability and functional impairment. Second, indices of DG proliferation and neurogenesis are changed 3 dpi in more severe TBI models relative to control animals (Dash et al, 2001;Chirumamilla et al, 2002;Peters et al, 2018;Villasana et al, 2019), but only a few papers look at DG neurogenesis at a shortterm time point post-mTBI, and the results are mixed (Wang et al, 2016;Neuberger et al, 2017;Tomura et al, 2020). To address this knowledge gap, the neurogenic regions of the DG (SGZ, GCL) from Sham and LFPI mice were assessed 3 dpi for indices of proliferation (Ki67+ and BrdU+ cell number) and neuroblasts/immature neurons (DCX+ cell number).…”

Section: Three Dpi: Neurogenesis Indices In the Ipsilateral Dg Neurogmentioning

confidence: 99%

“…These discrepancies are likely related in part to differences in experimental parameters, including time point post-TBI, "stage" of the process examined, approach to quantify the neurogenesis process, and TBI model used and its severity. To this end, it is notable that rodent models of mild brain injury -including lateral fluid percussion injury (LFPI), blast trauma, and weight dropalso produce mixed effects on the process of DG neurogenesis (Bye et al, 2011;Wang et al, 2016;Neuberger et al, 2017;Tomura et al, 2020). Given that new neuron replacement has been suggested as a potential treatment for TBI-induced cognitive dysfunction (Blaiss et al, 2011;Sun et al, 2015;Aertker et al, 2016;Sun, 2016), and the prevalence of mTBI in humans, it is surprising that only two rodent studies have examined injuryinduced effects on the process of DG neurogenesis after mTBI caused by LFPI.…”

Section: Introductionmentioning

confidence: 99%

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Mild Traumatic Brain Injury Induces Transient, Sequential Increases in Proliferation, Neuroblasts/Immature Neurons, and Cell Survival: A Time Course Study in the Male Mouse Dentate Gyrus

et al. 2021

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Mild traumatic brain injuries (mTBIs) are prevalent worldwide. mTBIs can impair hippocampal-based functions such as memory and cause network hyperexcitability of the dentate gyrus (DG), a key entry point to hippocampal circuitry. One candidate for mediating mTBI-induced hippocampal cognitive and physiological dysfunction is injury-induced changes in the process of DG neurogenesis. There are conflicting results on how TBI impacts the process of DG neurogenesis; this is not surprising given that both the neurogenesis process and the post-injury period are dynamic, and that the quantification of neurogenesis varies widely in the literature. Even within the minority of TBI studies focusing specifically on mild injuries, there is disagreement about if and how mTBI changes the process of DG neurogenesis. Here we utilized a clinically relevant rodent model of mTBI (lateral fluid percussion injury, LFPI), gold-standard markers and quantification of the neurogenesis process, and three time points post-injury to generate a comprehensive picture of how mTBI affects adult hippocampal DG neurogenesis. Male C57BL/6J mice (6-8 weeks old) received either sham surgery or mTBI via LFPI. Proliferating cells, neuroblasts/immature neurons, and surviving cells were quantified via stereology in DG subregions (subgranular zone [SGZ], outer granule cell layer [oGCL], molecular layer, and hilus) at short-term (3 days post-injury, dpi), intermediate (7 dpi), and long-term (31 dpi) time points. The data show this model of mTBI induces transient, sequential increases in ipsilateral SGZ/GCL proliferating cells, neuroblasts/immature neurons, and surviving cells which is suggestive of mTBI-induced neurogenesis. In contrast to these ipsilateral hemisphere findings, measures in the contralateral hemisphere were not increased in key neurogenic DG subregions after LFPI. Our work in this mTBI model is in line with most literature on other and more severe models of TBI in showing TBI stimulates the process of DG neurogenesis. However, as our DG data in mTBI provide temporal, subregional, and neurogenesis-stage resolution, these data are important to consider in regard to the functional importance of TBI-induction of the neurogenesis process and future work assessing the potential of replacing and/or repairing DG neurons in the brain after TBI.

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Section: Three Dpi: Neurogenesis Indices In the Ipsilateral Dg Neurogmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mild Traumatic Brain Injury Induces Transient, Sequential Increases in Proliferation, Neuroblasts/Immature Neurons, and Cell Survival: A Time Course Study in the Male Mouse Dentate Gyrus

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Therefore, examination of neurogenesis indices 3 dpi may reveal changes that influence the subsequent emergence of 7 dpi DG hyperexcitability and functional impairment. Second, indices of DG proliferation and neurogenesis are changed 3 dpi in more severe TBI models relative to control animals (Dash et al, 2001; Chirumamilla et al, 2002; Peters et al, 2018; Villasana et al, 2019), but only a few papers look at DG neurogenesis at an short-term time point post-mTBI, and the results are mixed (Wang et al, 2016; Neuberger et al, 2017; Tomura et al, 2020). To address this knowledge gap, the neurogenic regions of the DG (SGZ, GCL) from Sham and LFPI mice were assessed 3 dpi for indices of proliferation (Ki67+ and BrdU+ cell number) and neuroblasts/immature neurons (DCX+ cell number).…”

Section: Resultsmentioning

confidence: 99%

“…These discrepancies are likely related in part to differences in experimental parameters, including time point post-TBI, ‘stage’ of the process examined, approach to quantify the neurogenesis process, and TBI model used and its severity. To this end, it is notable that rodent models of mild brain injury - including lateral fluid percussion injury (LFPI), blast trauma, and weight drop - also produce mixed effects on the process of DG neurogenesis (Bye et al, 2011; Wang et al, 2016; Neuberger et al, 2017; Tomura et al, 2020). Given that new neuron replacement has been suggested as a potential treatment for TBI-induced cognitive dysfunction (Blaiss et al, 2011; Sun et al, 2015; Aertker et al, 2016; Sun, 2016), and the prevalence of mTBI in humans, it is surprising that only two rodent studies have examined injury-induced effects on the process of DG neurogenesis after mTBI caused by LFPI.…”

Section: Introductionmentioning

confidence: 99%

Mild traumatic brain injury induces transient, sequential increases in proliferation, neuroblasts/immature neurons, and cell survival: a time course study in the male mouse dentate gyrus

Clark

Yun

Acquah

et al. 2020

Preprint

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Mild traumatic brain injuries (mTBIs) are prevalent worldwide. mTBIs can impair hippocampal-based functions such as memory and cause network hyperexcitability of the dentate gyrus (DG), a key entry point to hippocampal circuitry. One candidate for mediating mTBI-induced hippocampal cognitive and physiological dysfunction is injury-induced changes in DG neurogenesis, a process that mediates spatial/contextual memory. There are conflicting results on how TBI impacts DG neurogenesis; this is not surprising given that both the neurogenesis process and the post-injury period are dynamic, and that neurogenesis quantification varies widely in the literature. Even within the minority of TBI studies focusing specifically on mild injuries, there is disagreement about if and how mTBI changes DG neurogenesis. Here we utilized a clinically-relevant rodent model of mTBI (lateral fluid percussion injury, LFPI), gold-standard neurogenesis markers and quantification approaches, and three time points post-injury to generate a comprehensive picture of how mTBI affects adult hippocampal DG neurogenesis. Male C57BL/6J mice (6-8 weeks old) received either sham surgery or mTBI via LFPI. Proliferating cells, neuroblasts/immature neurons, and surviving cells were quantified via stereology in DG subregions (subgranular zone [SGZ], outer granule cell layer [GCL], molecular layer, and hilus) at short-term (3 days post-injury, dpi), intermediate (7 dpi), and long-term (31 dpi) time points. The data suggest this model of mTBI induces transient, sequential increases in ipsilateral SGZ/GCL proliferating cells, immature neurons, and surviving cells which are indicative of mTBI-induced neurogenesis. In contrast to these ipsilateral hemisphere findings, measures in the contralateral hemisphere show no increase in neurogenesis indices in the key neurogenic DG subregions. Our work in this mTBI model is in line with the large fraction of literature that reports increased DG neurogenesis in other and more severe models of TBI. As our DG neurogenesis data in this mTBI model provide temporal, subregional, and neurogenesis-stage resolution, these data are important to consider in regard to the functional importance of TBI-induced neurogenesis and future work assessing the potential of replacing and/or repairing DG neurons in the brain after TBI.

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“…The setup for producing LISW, which is compact and easy to use and control, offers excellent safety and multifunctionality, as well as delivers site-selective shockwave application to laboratory animals at highly reproducible dose 5 , 11 – 14 . Furthermore, the positive pressure duration of the LISW used in this study was 0.6 s (Fig.…”

Section: Methodsmentioning

confidence: 99%

The cause of acute lethality of mice exposed to a laser-induced shock wave to the brainstem

Yamamura

Kiriu

Tomura

et al. 2022

Sci Rep

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Air embolism is generally considered the most common cause of death within 1 h of a blast injury. Shock lung, respiratory arrest, and circulatory failure caused by vagal reflexes contribute to fatal injuries that lead to immediate death; however, informative mechanistic data are insufficient. Here we used a laser-induced shock wave (LISW) to determine the mechanism of acute fatalities associated with blast injuries. We applied the LISW to the forehead, upper neck, and thoracic dorsum of mice and examined their vital signs. Moreover, the LISW method is well suited for creating site-specific damage. Here we show that only mice with upper neck exposure, without damage elsewhere, died more frequently compared with the other injured groups. The peripheral oxygen saturation (SpO2) of the former mice significantly decreased for < 1 min [p < 0.05] but improved within 3 min. The LISW exposure to the upper neck region was the most lethal factor, affecting the respiratory function. Protecting the upper neck region may reduce fatalities that are related to blast injuries.

show abstract

A novel mouse model of mild traumatic brain injury using laser-induced shock waves

Cited by 9 publications

References 31 publications

Mild Traumatic Brain Injury Induces Transient, Sequential Increases in Proliferation, Neuroblasts/Immature Neurons, and Cell Survival: A Time Course Study in the Male Mouse Dentate Gyrus

Mild Traumatic Brain Injury Induces Transient, Sequential Increases in Proliferation, Neuroblasts/Immature Neurons, and Cell Survival: A Time Course Study in the Male Mouse Dentate Gyrus

Mild traumatic brain injury induces transient, sequential increases in proliferation, neuroblasts/immature neurons, and cell survival: a time course study in the male mouse dentate gyrus

The cause of acute lethality of mice exposed to a laser-induced shock wave to the brainstem

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