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

Brain health is largely dependent on the metabolic regulation of amino acids. Brain injuries, diseases, and disorders can be detected through alterations in free amino acid (FAA) concentrations; and thus, mapping the changes has high diagnostic potential. Common methods focus on optimizing neurotran...

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Main Authors: Carly Norris, Justin Weatherbee, Susan F. Murphy, Pamela J. VandeVord
Format: Article
Language:English
Published: Elsevier 2024-01-01
Series:Neuroscience Research
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Online Access:http://www.sciencedirect.com/science/article/pii/S016801022300130X
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author Carly Norris
Justin Weatherbee
Susan F. Murphy
Pamela J. VandeVord
author_facet Carly Norris
Justin Weatherbee
Susan F. Murphy
Pamela J. VandeVord
author_sort Carly Norris
collection DOAJ
description Brain health is largely dependent on the metabolic regulation of amino acids. Brain injuries, diseases, and disorders can be detected through alterations in free amino acid (FAA) concentrations; and thus, mapping the changes has high diagnostic potential. Common methods focus on optimizing neurotransmitter quantification; however, recent focus has expanded to investigate the roles of molecular precursors in brain metabolism. An isocratic method using high performance liquid chromatography with electrochemical cell detection was developed to quantify a wide range of molecular precursors and neurotransmitters: alanine, arginine, aspartate, serine, taurine, threonine, tyrosine, glycine, glutamate, glutamine, and γ-Aminobutyric acid (GABA) following traumatic brain injury. First, baseline concentrations were determined in the serum, cerebrospinal fluid, hippocampus, cortex, and cerebellum of naïve male Sprague Dawley rats. A subsequent study was performed investigating acute changes in FAA concentrations following blast-induced traumatic brain injury (bTBI). Molecular precursor associated FAAs decreased in concentration at 4 h after injury in both the cortex and hippocampus while those serving as neurotransmitters remained unchanged. In particular, the influence of oxidative stress on the observed changes within alanine and arginine pathways following bTBI should be further investigated to elucidate the full therapeutic potential of these molecular precursors at acute time points.
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spelling doaj-art-c65103bd19d84adbb973e16408b60a1c2024-11-21T06:02:18ZengElsevierNeuroscience Research0168-01022024-01-011984756Quantifying acute changes in neurometabolism following blast-induced traumatic brain injuryCarly Norris0Justin Weatherbee1Susan F. Murphy2Pamela J. VandeVord3School of Biomedical Engineering and Sciences, Virginia Tech, Blacksburg, VA, USA; Department of Biomedical Engineering and Mechanics, Virginia Tech, Blacksburg VA, USADepartment of Biomedical Engineering and Mechanics, Virginia Tech, Blacksburg VA, USADepartment of Biomedical Engineering and Mechanics, Virginia Tech, Blacksburg VA, USA; Veterans Affairs Medical Center, Salem, VA, USASchool of Biomedical Engineering and Sciences, Virginia Tech, Blacksburg, VA, USA; Department of Biomedical Engineering and Mechanics, Virginia Tech, Blacksburg VA, USA; Veterans Affairs Medical Center, Salem, VA, USA; Corresponding author at: Department of Biomedical Engineering and Mechanics, Virginia Tech, 447 Kelly Hall, 325 Stanger St., Blacksburg, VA 24060, USA.Brain health is largely dependent on the metabolic regulation of amino acids. Brain injuries, diseases, and disorders can be detected through alterations in free amino acid (FAA) concentrations; and thus, mapping the changes has high diagnostic potential. Common methods focus on optimizing neurotransmitter quantification; however, recent focus has expanded to investigate the roles of molecular precursors in brain metabolism. An isocratic method using high performance liquid chromatography with electrochemical cell detection was developed to quantify a wide range of molecular precursors and neurotransmitters: alanine, arginine, aspartate, serine, taurine, threonine, tyrosine, glycine, glutamate, glutamine, and γ-Aminobutyric acid (GABA) following traumatic brain injury. First, baseline concentrations were determined in the serum, cerebrospinal fluid, hippocampus, cortex, and cerebellum of naïve male Sprague Dawley rats. A subsequent study was performed investigating acute changes in FAA concentrations following blast-induced traumatic brain injury (bTBI). Molecular precursor associated FAAs decreased in concentration at 4 h after injury in both the cortex and hippocampus while those serving as neurotransmitters remained unchanged. In particular, the influence of oxidative stress on the observed changes within alanine and arginine pathways following bTBI should be further investigated to elucidate the full therapeutic potential of these molecular precursors at acute time points.http://www.sciencedirect.com/science/article/pii/S016801022300130XBlastNeurotransmittersMolecular precursorsNeurometabolicHPLC
spellingShingle Carly Norris
Justin Weatherbee
Susan F. Murphy
Pamela J. VandeVord
Quantifying acute changes in neurometabolism following blast-induced traumatic brain injury
Neuroscience Research
Blast
Neurotransmitters
Molecular precursors
Neurometabolic
HPLC
title Quantifying acute changes in neurometabolism following blast-induced traumatic brain injury
title_full Quantifying acute changes in neurometabolism following blast-induced traumatic brain injury
title_fullStr Quantifying acute changes in neurometabolism following blast-induced traumatic brain injury
title_full_unstemmed Quantifying acute changes in neurometabolism following blast-induced traumatic brain injury
title_short Quantifying acute changes in neurometabolism following blast-induced traumatic brain injury
title_sort quantifying acute changes in neurometabolism following blast induced traumatic brain injury
topic Blast
Neurotransmitters
Molecular precursors
Neurometabolic
HPLC
url http://www.sciencedirect.com/science/article/pii/S016801022300130X
work_keys_str_mv AT carlynorris quantifyingacutechangesinneurometabolismfollowingblastinducedtraumaticbraininjury
AT justinweatherbee quantifyingacutechangesinneurometabolismfollowingblastinducedtraumaticbraininjury
AT susanfmurphy quantifyingacutechangesinneurometabolismfollowingblastinducedtraumaticbraininjury
AT pamelajvandevord quantifyingacutechangesinneurometabolismfollowingblastinducedtraumaticbraininjury