Cited by 163Traumatic Brain Injury and Neurovascular DisturbancesTraumatic Brain Injury ResearchNeuroscience and Neuropharmacology Research

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Glutamate Neurotransmission in Rodent Models of Traumatic Brain Injury

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Dorsett, Christopher R., McGuire, Jennifer L., DePasquale, Erica A. K., Gardner, Amanda E., Floyd, Candace L., McCullumsmith, Robert E.·2017·Journal of Neurotrauma

DOI 10.1089/neu.2015.4373PMC PMC5220558

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Abstract

Traumatic brain injury (TBI) is a leading cause of death and disability in people younger than 45 and is a significant public health concern. In addition to primary mechanical damage to cells and tissue, TBI involves additional molecular mechanisms of injury, termed secondary injury, that continue to evolve over hours, days, weeks, and beyond. The trajectory of recovery after TBI is highly unpredictable and in many cases results in chronic cognitive and behavioral changes. Acutely after TBI, there is an unregulated release of glutamate that cannot be buffered or cleared effectively, resulting in damaging levels of glutamate in the extracellular space. This initial loss of glutamate homeostasis may initiate additional changes in glutamate regulation. The excitatory amino acid transporters (EAATs) are expressed on both neurons and glia and are the principal mechanism for maintaining extracellular glutamate levels. Diffusion of glutamate outside the synapse due to impaired uptake may lead to increased extrasynaptic glutamate signaling, secondary injury through activation of cell death pathways, and loss of fidelity and specificity of synaptic transmission. Coordination of glutamate release and uptake is critical to regulating synaptic strength, long-term potentiation and depression, and cognitive processes. In this review, we will discuss dysregulation of extracellular glutamate and glutamate uptake in the acute stage of TBI and how failure to resolve acute disruptions in glutamate homeostatic mechanisms may play a causal role in chronic cognitive symptoms after TBI.

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Cell and Tissue Instructive Materials for Central Nervous System Repair
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“This is evidenced by the consistent finding that TBI impairs the expression of long-term potentiation (Giza and Prins, 2006; Schwarzbach et al., 2006; Dorsett et al., 2017).”
Background
Recovery of Olfactory Function After Excitotoxic Lesion of the Olfactory Bulbs Is Associated with Increases in Bulbar SIRT1 and SIRT4 Expressions
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Background
Astrocyte phenotypes: Emphasis on potential markers in neuroinflammation.
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“GLT1/ EAAT2 shows robust expression and specificity in astrocytes compared to GFAP (Lovatt et al., 2007); however, it is downregulated in the diseases associated with reactive gliosis (Verkhratsky et al., 2016; Dorsett et al., 2017).”
Background
Olfactory function in an excitotoxic model for secondary neuronal degeneration: Role of dopaminergic interneurons.
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Tetramerization of PKM2 Alleviates Traumatic Brain Injury by Ameliorating Mitochondrial Damage in Microglia
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“The secondary stage is triggered by the initial injury and includes excitotoxicity, mitochondrial dysfunction, and neuroinflammation (Anthonymuthu et al. 2016, Dorsett et al. 2017, Jassam et al. 2017).”
Ectoderm-derived frontal bone mesenchymal stem cells promote traumatic brain injury recovery by alleviating neuroinflammation and glutamate excitotoxicity partially via FGF1
Qin, Q., Wang, T., Xu, Z., Liu, S., Zhang, H., Du, Z., Wang, J., Wang, Y., Wang, Z., Yuan, S., et al. (2022) · Stem Cell Research & Therapy · doi:10.1186/s13287-022-03032-6 · Cited by 22
“External trauma might cause structural damage, oxidative stress, excessive excitatory neurotransmitters [3], and an inflammatory cascade responsible for further cell death [4], leading to anatomical and functional brain damage.”
Galantamine protects against synaptic, axonal, and vision deficits in experimental neurotrauma
Naguib, S., Bernardo-Colón, A., Cencer, C. S., Gandra, N., & Rex, T. S. (2019) · Neurobiology of Disease · doi:10.1016/j.nbd.2019.104695 · Cited by 17
“(Dorsett et al., 2017) Additionally, TBI in rats results in excess glutamate followed by a down-regulation in expression of GLAST and EAAT1 in glial cells.”
Why Does Brain Trauma Research Fail?
Alves, J. L., Rato, J. R., & da Silva, V. M. M. (2019) · World Neurosurgery · doi:10.1016/j.wneu.2019.06.212 · Cited by 26
Vascular and non‐vascular contributors to memory reduction during traumatic brain injury
Charkviani, M., Muradashvili, N., & Lominadze, D. G. (2019) · European Journal of Neuroscience · doi:10.1111/ejn.14390 · Cited by 17
“During moderate to severe TBI levels of extracellular glutamate are increased (Dorsett et al., 2017; Guerriero, Giza, & Rotenberg, 2015), leading to enhanced calcium influx through hyperactivation of NMDARs, resulting in calcium overload and neurodegeneration due to excitotoxicity (Hardingham, 2009).”
Background
Traumatic brain injury impairs sensorimotor function in mice
Sackheim, A. M., Stockwell, D. W., Villalba, N., Haines, L., Scott, C., Russell, S., Hammack, S. E., & Freeman, K. (2017) · Journal of Surgical Research · doi:10.1016/j.jss.2017.02.016 · Cited by 17
Cellular senescence as a key contributor to secondary neurodegeneration in traumatic brain injury and stroke
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Targeting the adenosine A2A receptor for neuroprotection and cognitive improvement in traumatic brain injury and Parkinson's disease
Zhao, Y., Zhou, Y., & Chen, J. (2023) · Chinese Journal of Traumatology · doi:10.1016/j.cjtee.2023.08.003 · Cited by 21
“Adenosine, acting via A 2A R, exerts neuromodulation of secondary injuries and in ﬂ uences the outcomes and sequelae of TBI by neuroin ﬂ ammation 84 e 86 , BBB impairment 68 , controlling glutamate-induced excitotoxicity 87 , autophagy blocking and lipid peroxidation 88 .”
Background
Polygalasaponin F protects hippocampal neurons against glutamate-induced cytotoxicity
Li, B., Sun, C., Cao, X.-C., Liu, Z., & Ma, C. (2021) · Neural Regeneration Research · doi:10.4103/1673-5374.314321 · Cited by 18
“Furthermore, glutamate excitotoxicity-induced neuronal death is one of the major pathogenic mechanisms underlying these neurological disorders (Lau and Tymianski, 2010; Mehta et al., 2013; Huberfeld and Vecht, 2016; Dorsett et al., 2017; Jiang et al., 2019; Chu et al., 2020).”
Background
Improving Sensitivity and Longevity of In Vivo Glutamate Sensors with Electrodeposited NanoPt
Robbins, E. M., Wong, B., Pwint, M. Y., Salavatian, S., Mahajan, A., & Cui, X. T. (2024) · ACS Applied Materials & Interfaces · doi:10.1021/acsami.4c06692 · Cited by 15
Prion-Like Propagation Mechanisms in Tauopathies and Traumatic Brain Injury: Challenges and Prospects
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Supplement and nutraceutical therapy in traumatic brain injury
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“For example, EAAT2 knockout led to life-threatening spontaneous seizures and substantial neuronal loss in mice, whereas functional EAAT2 prevented post-traumatic seizures in rat models of brain trauma (Dorsett et al., 2017; Liu et al., 2020).”
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Background
Acute effects of single and repeated mild traumatic brain injury on levels of neurometabolites, lipids, and mitochondrial function in male rats
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Molecular Toxicology and Pathophysiology of Comorbid Alcohol Use Disorder and Post-Traumatic Stress Disorder Associated with Traumatic Brain Injury
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“The coordination of glutamate release and uptake is critical to regulating synaptic strength, long-term potentiation, depression, and cognitive processes in chronic TBI [97].”
Background
Saffron Extract Attenuates Anxiogenic Effect and Improves Cognitive Behavior in an Adult Zebrafish Model of Traumatic Brain Injury
Chaoul, V., Awad, M., Harb, F., Najjar, F., Hamadé, A., Nabout, R. A. E., & Soueid, J. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms231911600 · Cited by 11
“secondary insult [8], leading to an increased level of intracellular calcium.”
Background
Enhancement of intrinsic neuronal excitability‐mediated by a reduction in hyperpolarization‐activated cation current (Ih) in hippocampal CA1 neurons in a rat model of traumatic brain injury
Karimi, S. A., Hosseinmardi, N., Sayyah, M., Hajisoltani, R., & Janahmadi, M. (2020) · Hippocampus · doi:10.1002/hipo.23270 · Cited by 18
“early stages of TBI induction, extracellular glutamate levels increase (Cantu et al., 2014; Dorsett et al., 2017; Hinzman et al., 2010), this, in turn, may cause a reduction in Ih current and thereby promote neuronal hyperexcitability (Balakrishnan & Mironov, 2018).”
Background
Ultrasound Imaging Comparison of Crural Fascia Thickness and Muscle Stiffness in Stroke Patients with Spasticity
Choi, J., Do, Y., & Lee, H. (2024) · Diagnostics · doi:10.3390/diagnostics14222606 · Cited by 10
“Post-brain-injury changes in neurotransmitter levels cause pathological changes in the fascia [13].”
NMDAR (2C) deletion in astrocytes relieved LPS-induced neuroinflammation and depression
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Repetitive mild traumatic brain injury induces persistent alterations in spontaneous synaptic activity of hippocampal CA1 pyramidal neurons
Langlois, L. D., Selvaraj, P., Simmons, S. C., Gouty, S., Zhang, Y., & Nugent, F. S. (2022) · IBRO Neuroscience Reports · doi:10.1016/j.ibneur.2022.02.002 · Cited by 15
“158 the long-term impairment of cognitive function following TBI may be attributable to an imbalance of synaptic transmission following a persistent deficit in extracellular glutamate regulation resulting in prolonged elevated levels of glutamate at synapses (Dorsett et al., 2017).”
Background
Catastrophic consequences: can the feline parasite Toxoplasma gondii prompt the purrfect neuroinflammatory storm following traumatic brain injury?
Baker, T. L., Sun, M., Semple, B. D., Tyebji, S., Tonkin, C. J., Mychasiuk, R., & Shultz, S. R. (2020) · Journal of Neuroinflammation · doi:10.1186/s12974-020-01885-3 · Cited by 11
The roles of neuroinflammation and glutamatergic excitotoxicity in treatment-resistant depression
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Unveiling Leukocyte Extracellular Traps in Inflammatory Responses of the Central Nervous System
Colciaghi, F., & Costanza, M. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.915392 · Cited by 9
Effect of Xenon on Proinflammatory Activation and Apoptosis of Human Neutrophils Under Ex Vivo Conditions
Grebenchikov, O., Shabanov, A., Nikolayev, L. L., Shpichko, A., Bratishchev, I. V., Marchenko, L., Khusainov, S. Z., Cherpakov, R., & Shpichko, N. P. (2021) · Russian Sklifosovsky Journal "Emergency Medical Care" · doi:10.23934/2223-9022-2021-10-3-511-520 · Cited by 9
Riluzole attenuates acute neural injury and reactive gliosis, hippocampal-dependent cognitive impairments and spontaneous recurrent generalized seizures in a rat model of temporal lobe epilepsy
Kyllo, T., Allocco, D., Hei, L. V., Wulff, H., & Erickson, J. D. (2024) · Frontiers in Pharmacology · doi:10.3389/fphar.2024.1466953 · Cited by 9
The mGluR5‐mediated Arc activation protects against experimental traumatic brain injury in rats
Chen, T., Li, Y.-F., Ren, X., & Wang, Y.-H. (2024) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.14695 · Cited by 8
“6 In human, elevated levels of glutamate in cerebrospinal fluid (CSF) can be observed after TBI, which might persist for days and weeks.”
Effect of drug therapy on nerve repair of moderate-severe traumatic brain injury: A network meta-analysis
Li, M., Huo, X., Wang, Y., Li, W., Xiao, L., Jiang, Z.-F., Han, Q., Su, D., Chen, T., & Xia, H. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.1021653 · Cited by 8
“This is known as secondary injury (Winkler et al., 2016; Dorsett et al., 2017; Simon et al., 2017; Sorby-Adams et al., 2017).”
Intervention of CXCL5 attenuated neuroinflammation and promoted neurological recovery after traumatic brain injury
Li, L., Zhou, J.-P., Han, L.-Y., Guo, C., Ma, S.-Y., Ge, S.-N., & Qu, Y. (2024) · NeuroReport · doi:10.1097/wnr.0000000000002032 · Cited by 7
Trends and hotspots in research of traumatic brain injury from 2000 to 2022: A bibliometric study
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Chalcone-Derived Nrf2 Activator Protects Cognitive Function via Maintaining Neuronal Redox Status
Cui, Y., Xiong, Y., Li, H., Zeng, M., Wang, Y., Li, Y., Zou, X., Lv, W., Gao, J., Cao, R., et al. (2021) · Antioxidants · doi:10.3390/antiox10111811 · Cited by 8
RNA-seq analysis and compound screening highlight multiple signalling pathways regulating secondary cell death after acute CNS injury in vivo
Herzog, C. M. S., Greenald, D., Larraz, J., Keatinge, M., & Herrgen, L. (2020) · Biology Open · doi:10.1242/bio.050260 · Cited by 7
“With NMDA receptors acting as key mediators of excitotoxicity (Dorsett et al., 2017), it is plausible that polyamines could regulate excitotoxic cell death after acute neural injury.”
Background
Intranasal Leukemia Inhibitory Factor Attenuates Gliosis and Axonal Injury and Improves Sensorimotor Function After a Mild Pediatric Traumatic Brain Injury
D’Mello, V., Subramaniam, M., Bhalla, A. P., Saavedra, S., Leiba, O., & Levison, S. (2023) · Neurotrauma Reports · doi:10.1089/neur.2021.0075 · Cited by 6
“34,35 This scenario is reminiscent of pre-conditioning where a mild insult subsequently reduces the extent of injury induced by more severe injury, which correlates with increased expression of GFAP, glutamine synthetase, GLAST, monocarboxylate transporter-1, and ceruloplasmin.”
Brivaracetam prevents the development of epileptiform activity when administered early after cortical neurotrauma in rats
Ling, D. S. F., Yang, L., & Goodman, J. (2022) · Epilepsia · doi:10.1111/epi.17167 · Cited by 6
Physical Exercise as a Modulator of Vascular Pathology and Thrombin Generation to Improve Outcomes After Traumatic Brain Injury
Papalia, W. L., Nascimento, A. S., Krishna, G., Cunha, N. B., Furian, A. F., Oliveira, M. S., Royes, L. F. F., & Fighera, M. R. (2021) · Molecular Neurobiology · doi:10.1007/s12035-021-02639-9 · Cited by 6
“After TBI, the excitotoxicity evidenced by extracellular glutamate increase is a major contributing factor in apoptosis and neuronal death [52, 53].”
Background
A novel missense variant in GPT2 causes non-syndromic autosomal recessive intellectual disability in a consanguineous Iranian family.
Binaafar, S., Razmara, E., Mahdieh, N., Sahebjame, H., Tavasoli, A., & Garshasbi, M. (2020) · European Journal of Medical Genetics · doi:10.1016/j.ejmg.2020.103853 · Cited by 6
Mild traumatic brain injury gives rise to chronic depression-like behavior and associated alterations in glutamatergic protein expression
Talty, C.-E., Murphy, S. F., & VandeVord, P. J. (2024) · Neuroscience · doi:10.1016/j.neuroscience.2024.09.039 · Cited by 6
“Glutamate excitotoxicity is a well-studied consequence of TBI which involves mass amounts of glutamate efflux into the synapse upon the mechanical force of injury (Dorsett et al., 2017; Giza and Hovda, 2014).”
Brain Injury Effects on Neuronal Activation and Synaptic Transmission in the Basolateral Amygdala of Adult Male and Female Wistar Rats
Jacotte-Simancas, A., Middleton, J. W., Stielper, Z. F., Edwards, S., Molina, P. E., & Gilpin, N. W. (2022) · Journal of Neurotrauma · doi:10.1089/neu.2021.0270 · Cited by 4
“61,62 Diffuse injury results in widespread damage in the brain that affects axons, vasculature, and hypoxia.”
Evodiamine attenuates neurological impairment by inducing PANoptosis in microglia after severe traumatic brain injury
Zheng, H., Tian, X., Wang, Y., Ye, X., Ren, X., Gu, Y., Wang, J., Zheng, G., & Yang, X. (2025) · Pharmacological Research · doi:10.1016/j.phrs.2025.108034 · Cited by 5
Significance of NMDA receptor-targeting compounds in neuropsychological disorders: An in-depth review
Forouzanfar, F., Ahmadzadeh, A. M., Pourbagher‐Shahri, A. M., & Gorji, A. (2025) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2025.177690 · Cited by 4
mNSCs overexpressing Rimkla transplantation facilitates cognitive recovery in a mouse model of traumatic brain injury
Ji, T., Pang, Y., Cheng, M., Wang, R., Chen, X., Zhang, C., Liu, M., Zhang, J., & Zhong, C. (2023) · iScience · doi:10.1016/j.isci.2023.107913 · Cited by 5

Authors: Dorsett, C. R., McGuire, J. L., DePasquale, E. A. K., Gardner, A. E., Floyd, C. L., & McCullumsmith, R. E.
Affiliations: University of North Carolina at Chapel Hill (US)
University of Cincinnati (US)
University of Alabama at Birmingham (US)
Corresponding author: McCullumsmith, Robert E.
ORCID: McGuire, Jennifer L.
DePasquale, Erica A. K.
Floyd, Candace L.
McCullumsmith, Robert E.
Venue: Journal of Neurotrauma
Publisher: SAGE Publications
Published: 2017-01
Volume: 34
Issue: 2
Pages: 263-272
ISSN: 0897-7151 (ISSN-L)
1557-9042
DOI: 10.1089/neu.2015.4373
PMC: PMC5220558
OpenAlex: W2494112084
Cited by: 163
References: 0
Citations by year: 2026: 15 · 2025: 11 · 2024: 26 · 2023: 16 · 2022: 22 · 2021: 22 · 2020: 16 · 2019: 15 · 2018: 12 · 2017: 6
FWCI: 1.57
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: journals.sagepub.com/page/policies/text-and-data-mining-license (tdm)
Locations: Journal of Neurotrauma (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
UNC Libraries
Funders: National Institute of Mental Health (R01MH094445, R01MH107487)
National Institute of Neurological Disorders and Stroke (R01NS075162)
Topics: Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords: traumatic brain injury, glutamatergic neurotransmission, glutamate transporters, glutamate homeostasis, secondary injury, excitotoxicity, synaptic transmission, long-term potentiation and depression, rodent models
MeSH terms: Brain Injuries, Traumatic, Animals, Disease Models, Animal, Humans, Synaptic Transmission, Neuroglia, Rodentia, Synapses, Signal Transduction, Glutamic Acid, Glutamate Plasma Membrane Transport Proteins, Mice, Rats

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Glutamate Neurotransmission in Rodent Models of Traumatic Brain Injury

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