ArticleNeurochemistry international2018
Early behavioral and metabolomic change after mild to moderate traumatic brain injury in the developing brain.
Article in Neurochemistry international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 26 citations in OpenAlex.
- Metabolic-driven analytics of traumatic brain injury and neuroprotection by ethyl pyruvate.Journal of neuroinflammation · 2024Article
- A Systematic Review of Traumatic Brain Injury in Modern Rodent Models: Current Status and Future Prospects.Biology · 2024Review
- An overview of preclinical models of traumatic brain injury (TBI): relevance to pathophysiological mechanisms.Frontiers in cellular neuroscience · 2024Review
- Cerebrospinal fluid metabolite alterations in patients with different etiologies, diagnoses, and prognoses of disorders of consciousness.Brain and behavior · 2023Article
- What Happens in TBI? A Wide Talk on Animal Models and Future Perspective.Current neuropharmacology · 2023Review
- Article
- Neonatal encephalopathy plasma metabolites are associated with neurodevelopmental outcomes.Pediatric research · 2022Article
- Melatonin alleviates traumatic brain injury-induced anxiety-like behaviors in rats: Roles of the protein kinase A/cAMP-response element binding signaling pathway.Experimental and therapeutic medicine · 2022Article
- Supraspinal Sensorimotor and Pain-Related Reorganization after a Hemicontusion Rat Cervical Spinal Cord Injury.Journal of neurotrauma · 2021Article
- Traumatic brain injury induces region-specific glutamate metabolism changes as measured by multiple mass spectrometry methods.iScience · 2021Article
- Impact of pediatric traumatic brain injury on hippocampal neurogenesis.Neural regeneration research · 2021Review
- Metabolic Abnormalities in Patients with Chronic Disorders of Consciousness.Aging and disease · 2021Article
- Traumatic brain injury metabolome and mitochondrial impact after early stage Ru360 treatment.Mitochondrion · 2021Article
- Organophosphorus flame retardants are developmental neurotoxicants in a rat primary brainsphere in vitro model.Archives of toxicology · 2021Article
- Association Between Magnetic Resonance Imaging-Based Spinal Morphometry and Sensorimotor Behavior in a Hemicontusion Model of Incomplete Cervical Spinal Cord Injury in Rats.Brain connectivity · 2020Article
- Kaempferol Treatment after Traumatic Brain Injury during Early Development Mitigates Brain Parenchymal Microstructure and Neural Functional Connectivity Deterioration at Adolescence.Journal of neurotrauma · 2020Article
- Metabolomics Analysis of Hippocampus and Cortex in a Rat Model of Traumatic Brain Injury in the Subacute Phase.Frontiers in neuroscience · 2020Article
- Animal Models of Traumatic Brain Injury and Assessment of Injury Severity.Molecular neurobiology · 2019Review
- Beneficial Effects of Kaempferol after Developmental Traumatic Brain Injury Is through Protection of Mitochondrial Function, Oxidative Metabolism, and Neural Viability.Journal of neurotrauma · 2019Article
- Consolidated Biochemical Profile of Subacute Stage Traumatic Brain Injury in Early Development.Frontiers in neuroscience · 2019Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Pathophysiology of developmental traumatic brain injury (TBI) is unique due to intrinsic differences in the developing brain. Energy metabolic studies of the brain during early development (P13 to P30) have indicated acute oxidative energy metabolic decreases below 24 h after TBI, which generally recovered by 48 h. However, marked neurodegeneration and altered neural functional connectivity have been observed at later stages into adolescence. As secondary neurodegeneration is most prominent during the first week after TBI in the rat model, we hypothesized that the subacute TBI-metabolome may contain predictive markers of neurodegeneration. Sham and TBI metabolomes were examined at 72 h after a mild to moderate intensity TBI in male Sprague-Dawley rats aged P31. Sensorimotor behavior was assessed at 24, 48 and 72 h after injury, followed by 72-hour postmortem brain removal for metabolomics using Liquid Chromatography/Mass Spectrometry (LC-MS) measurement. Broad TBI-induced metabolomic shifts occurred with relatively higher intensity in the injury-lateralized (ipsilateral) hemisphere. Intensity of metabolomic perturbation correlated with the extent of sensorimotor behavioral deficit. N-acetyl-aspartate (NAA) levels at 72 h after TBI, predicted the extent of neurodegeneration assessed histochemically 7-days post TBI. Results from the multivariate untargeted approach clearly distinguished metabolomic shifts induced by TBI. Several pathways including amino acid, fatty acid and energy metabolism continued to be affected at 72 h after TBI, whose collective effects may determine the overall pathological response after TBI in early development including neurodegeneration.
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