A novel model of blast induced traumatic brain injury caused by compressed gas produced sustained cognitive deficits in rats: involvement of phosphorylation of tau at the Thr205 epitope

Shi, Qi; Chen, Bing; Nie, Chuang; Zhao, Zhiping; Jun-hai, Zhao; Si, Shao-yan; Cui, Shaojie; J, Gu

doi:10.1016/j.brainresbull.2020.02.002

Cited by 19 publications

(6 citation statements)

References 42 publications

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“…Similarly, we observed prolonged cognitive deficits in our blast injury model. A week after injury, spatial recognition was impaired in the NOR and Y maze tasks, consistent with low cognitive performance in other blast injury models at seven days post-SBI in the Y maze (67, 68) and other cognitive tasks (69)(70)(71). Our study found prolonged impairment in NOR during the fourth week after SBI, consistent with poor memory performance impairment thirty days post-injury in the Barnes maze (70, 72).…”

Section: Discussionsupporting

confidence: 85%

Dexmedetomidine-mediated sleep phase modulation ameliorates motor and cognitive performance in a chronic blast-injured mouse model

Bibineyshvili

Schiff²,

Calderon³

2022

Front. Neurol.

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Multiple studies have shown that blast injury is followed by sleep disruption linked to functional sequelae. It is well established that improving sleep ameliorates such functional deficits. However, little is known about longitudinal brain activity changes after blast injury. In addition, the effects of directly modulating the sleep/wake cycle on learning task performance after blast injury remain unclear. We hypothesized that modulation of the sleep phase cycle in our injured mice would improve post-injury task performance. Here, we have demonstrated that excessive sleep electroencephalographic (EEG) patterns are accompanied by prominent motor and cognitive impairment during acute stage after secondary blast injury (SBI) in a mouse model. Over time we observed a transition to more moderate and prolonged sleep/wake cycle disturbances, including changes in theta and alpha power. However, persistent disruptions of the non-rapid eye movement (NREM) spindle amplitude and intra-spindle frequency were associated with lasting motor and cognitive deficits. We, therefore, modulated the sleep phase of injured mice using subcutaneous (SC) dexmedetomidine (Dex), a common, clinically used sedative. Dex acutely improved intra-spindle frequency, theta and alpha power, and motor task execution in chronically injured mice. Moreover, dexmedetomidine ameliorated cognitive deficits a week after injection. Our results suggest that SC Dex might potentially improve impaired motor and cognitive behavior during daily tasks in patients that are chronically impaired by blast-induced injuries.

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Section: Discussionsupporting

confidence: 85%

Dexmedetomidine-mediated sleep phase modulation ameliorates motor and cognitive performance in a chronic blast-injured mouse model

Bibineyshvili

Schiff²,

Calderon³

2022

Front. Neurol.

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“…Tau protein is a member of the microtubule-associated protein family [30]. The phosphorylated tau aggregates further form neurofibrillary tangles (NFT), which have been considered a common pathological feature of many neurodegenerative diseases and TBI [31]. It's reported that NFT was present in the mice brain after 3-4 months of chronic repetitive mild traumatic brain injury [32].…”

Section: Discussionmentioning

confidence: 99%

A novel simple traumatic brain injury mouse model

Chen

Hou

et al. 2022

Chin Neurosurg Jl

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Background Traumatic brain injury, one of the leading causes of death in adults under 40 years of age in the world, is frequently caused by mechanical shock, resulting in diffuse neuronal damage and long-term cognitive dysfunction. Many existing TBI animal models revival with expensive equipment or special room are needed or the processes of operations are complex and not easy to be widely used. Therefore, a simpler TBI model needs to be designed. Methods Our TBI model is an innovation of the modeling method through air guns shutting rubber bullets. A core facet is the application of our designed rubber bullet impact device. It could focus the hitting power to the fixed site of the brain, thus triggering a mild closed head injury. Moreover, the degree of damage can be adjusted by the times of shots. Results Our model induced blood-brain barrier leakage and diffused neuronal damage. Besides, it led to an increased level of Tau phosphorylation and resulted in cognitive dysfunction within several weeks post-injury. Conclusion Our TBI model is not only simple and time-saving but also can simulate mild brain injuries in clinical. It is suitable for exploring pathobiological mechanisms as well as a screening of potential therapies for TBI.

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“…In connection with this, now experimental studies to establish biological (biochemical, molecular, cellular, tissue, functional, behavioral) markers of blastinduced brain injury are gaining momentum [7]. In particular, on the 1st day of the post-traumatic period, macroscopic cerebral edema was detected but the hemorrhage was not determined [8]. Microscopically, blood-brain barrier (BBB) damage, changes in neuronal density, axonal damage and progressive myelin loss are detected [2, 9, 10].…”

Section: /том Xxix/1mentioning

confidence: 99%

Histopathological and ultrastructural changes in the rats brain after air shock wave impact

Kozlov,

Kozlova,

Bondarenko

et al. 2024

Med. perspekt.

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The using of explosive substances and devices can lead to brain injuries, the diagnosis of which requires the determination of primary biomarkers. Therefore, the aim was to establish and study histopathological and ultrastructural changes in the rats brain after exposure to an air blast wave. The study was carried out on 18 male Wistar rats, which were randomly divided into two groups: sham (n=9) and experimental (n=9). The animals of the experimental group were anesthetized with halothane and gently fixed in a horizontal position on the abdomen with the front part of the rat's muzzle at a distance of 5 cm from the device opening and subjected to an excess pressure of 26-36 kPa. Animals of both groups were decapitated, brains were removed, fixed, histopathological and ultrastructural analyzes were conducted using standard methods. Intergroup differences were assessed by Mann-Whitney U-test. Light microscopy revealed primary lesions in the form of small focal, multifocal hemorrhages, cerebral vessel ruptures and microscopic ruptures of the brain substance. In almost all brain samples, there is a significant saturation of the venous vessels with the presence of erythrocyte stasis. Violation of the blood-brain barrier, the presence of edema of the perivascular space, and petechial hemorrhages in the neuropil were registered ultrastructurally. Based on the study results, a morphological algorithm for assessing primary histostructural intracranial brain injuries and their consequences after exposure to an air shock wave was proposed. The injuries were found to be caused by the direct traumatic effect of the air shock wave. In the acute post-traumatic period, histopathological and ultrastructural changes in the brain can manifest as changes in neurons and in the blood-brain barrier and be accompanied by perivascular multifocal small-focal hemorrhages, neuropil ruptures, edema of pericellular and perivascular spaces, which together can be considered as biomarkers of primary traumatic changes after exposure to an air shock wave.

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A novel model of blast induced traumatic brain injury caused by compressed gas produced sustained cognitive deficits in rats: involvement of phosphorylation of tau at the Thr205 epitope

Cited by 19 publications

References 42 publications

Dexmedetomidine-mediated sleep phase modulation ameliorates motor and cognitive performance in a chronic blast-injured mouse model

Dexmedetomidine-mediated sleep phase modulation ameliorates motor and cognitive performance in a chronic blast-injured mouse model

A novel simple traumatic brain injury mouse model

Histopathological and ultrastructural changes in the rats brain after air shock wave impact

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