Quantifying acute changes in neurometabolism following blast-induced traumatic brain injury

Norris, Carly; Weatherbee, James A.; Murphy, Susan; VandeVord, Pamela J.

doi:10.1016/j.neures.2023.06.008

Cited by 4 publications

(3 citation statements)

References 55 publications

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“…We also found the brain itself diffuse damage, which causes an inflammatory process involving neutrophils. Comparing our results with previous studies which are showing an existing systemic cytokine response to mild blast-induced traumatic brain injury, we think that an active inflammatory response is unfolding [21,23,27]. All of these changes, both individually and in combination, require the launch of compensatory mechanisms to maintain the brain functional activity [13].…”

Section: Discussionsupporting

confidence: 79%

Changes of rat’s brain vesseles after air shock wave exposure

Kozlova,

Kozlov,

Maslak

et al. 2024

Rep. of Morph.

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Mild blast-induced traumatic brain injury is common among the military, resulting in cognitive impairment, reduced socialization, which leads to disability and, as a result, a deterioration in the quality of life. It is considered that blood-brain barrier disruption and microvascular dysfunction are the key to this type of injury. The purpose of study was to study changes in brain vessels after air shock wave exposure. The study was carried out on 48 mature male Wistar rats, which were randomly divided into 2 groups: an experimental group, in which animals were subjected to inhalation anesthesia using halothane and exposed to a shock wave with an overpressure of 26.4±3.6 kPa, and a Sham group. After simulation of injury on days 1st, 3rd, 7th, 14th, and 21st, the rats were euthanized and the brain was removed and after all subjected to standard histological procedures and stained with hematoxylin and eosin. For immunohistochemical studies, as primary antibodies were used eNOS. The finished preparations were examined by light microscopy and photographed. Disorders of the cerebral vessels in experimental rats were detected from day 1st of the posttraumatic period. It was found that the blast wave led to vascular rupture, as well as increased vascular permeability with diapedesis of red blood cells and cerebral edema for up to 21st days. Focal violations of the vascular wall integrity in cortical and hippocampal hemocapillaries, venular link of the submembrane vessels; changes in the morphology of the metabolic vessels endothelium; uneven blood filling of the brain vessels were of major importance. These changes indicate that increased eNOS expression leads to dilation of cerebral vessels, which is a compensatory mechanism in response to injury to improve cerebral blood circulation. However, eNOS is not involved in vasodilation, which we observed up to 21st day post-trauma.

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Section: Discussionsupporting

confidence: 79%

Changes of rat’s brain vesseles after air shock wave exposure

Kozlova,

Kozlov,

Maslak

et al. 2024

Rep. of Morph.

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“…A study by Kumari et al (2023) also showed an Alanine (Ala) reduction in the hippocampus 24 h postmild, moderate, and repeated bTBI, which aligns with another study by Norris et al (2023). This study, quantifying acute changes after bTBI in the metabolism of free amino acids as molecular precursors, neurotransmitters and metabolic regulators 10.3389/fncel.2024.1335849 in rats, found alterations in Arg and Ala pathways linked to oxidative stress following bTBI (Norris et al, 2023). Decreased Arg may elevate oxidative stress via NOS and contribute to proinflammatory cascades (Mader and Czorlich, 2022).…”

Section: The Role Of Senescent Glial Cells In Traumatic Brain Injury ...supporting

confidence: 84%

“…These metabolic shifts may affect biochemical processes and metabolic-dependent mechanisms such as the epigenome, highlighting the intricate link between metabolism and epigenetics ( Kumari et al, 2023 ). A study by Kumari et al (2023) also showed an Alanine (Ala) reduction in the hippocampus 24 h post-mild, moderate, and repeated bTBI, which aligns with another study by Norris et al (2023) . This study, quantifying acute changes after bTBI in the metabolism of free amino acids as molecular precursors, neurotransmitters and metabolic regulators in rats, found alterations in Arg and Ala pathways linked to oxidative stress following bTBI ( Norris et al, 2023 ).…”

Section: Traumatic Brain Injury In Military and Veterans And Special ...supporting

confidence: 84%

Reactive gliosis in traumatic brain injury: a comprehensive review

Amlerova,

Chmelova,

Anderova

et al. 2024

Front. Cell. Neurosci.

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Traumatic brain injury (TBI) is one of the most common pathological conditions impacting the central nervous system (CNS). A neurological deficit associated with TBI results from a complex of pathogenetic mechanisms including glutamate excitotoxicity, inflammation, demyelination, programmed cell death, or the development of edema. The critical components contributing to CNS response, damage control, and regeneration after TBI are glial cells–in reaction to tissue damage, their activation, hypertrophy, and proliferation occur, followed by the formation of a glial scar. The glial scar creates a barrier in damaged tissue and helps protect the CNS in the acute phase post-injury. However, this process prevents complete tissue recovery in the late/chronic phase by producing permanent scarring, which significantly impacts brain function. Various glial cell types participate in the scar formation, but this process is mostly attributed to reactive astrocytes and microglia, which play important roles in several brain pathologies. Novel technologies including whole-genome transcriptomic and epigenomic analyses, and unbiased proteomics, show that both astrocytes and microglia represent groups of heterogenic cell subpopulations with different genomic and functional characteristics, that are responsible for their role in neurodegeneration, neuroprotection and regeneration. Depending on the representation of distinct glia subpopulations, the tissue damage as well as the regenerative processes or delayed neurodegeneration after TBI may thus differ in nearby or remote areas or in different brain structures. This review summarizes TBI as a complex process, where the resultant effect is severity-, region- and time-dependent and determined by the model of the CNS injury and the distance of the explored area from the lesion site. Here, we also discuss findings concerning intercellular signaling, long-term impacts of TBI and the possibilities of novel therapeutical approaches. We believe that a comprehensive study with an emphasis on glial cells, involved in tissue post-injury processes, may be helpful for further research of TBI and be the decisive factor when choosing a TBI model.

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Spatial Intracranial Pressure Fields Driven by Blast Overpressure in Rats

Norris,

Murphy,

Talty

et al. 2024

Ann Biomed Eng

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Free-field blast exposure imparts a complex, dynamic response within brain tissue that can trigger a cascade of lasting neurological deficits. Full body mechanical and physiological factors are known to influence the body’s adaptation to this seemingly instantaneous insult, making it difficult to accurately pinpoint the brain injury mechanisms. This study examined the intracranial pressure (ICP) profile characteristics in a rat model as a function of blast overpressure magnitude and brain location. Metrics such as peak rate of change of pressure, peak pressure, rise time, and ICP frequency response were found to vary spatially throughout the brain, independent of blast magnitude, emphasizing unique spatial pressure fields as a primary biomechanical component to blast injury. This work discusses the ICP characteristics and considerations for finite element models, in vitro models, and translational in vivo models to improve understanding of biomechanics during primary blast exposure.

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Quantifying acute changes in neurometabolism following blast-induced traumatic brain injury

Cited by 4 publications

References 55 publications

Changes of rat’s brain vesseles after air shock wave exposure

Changes of rat’s brain vesseles after air shock wave exposure

Reactive gliosis in traumatic brain injury: a comprehensive review

Spatial Intracranial Pressure Fields Driven by Blast Overpressure in Rats

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