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Glutamate receptor and traumatic brain injury

Mihir V Patel, Emily Sewell, Samantha Dickson, Hyuck Kim, David Meaney, Bonnie L Firestein
Postsynaptic density 95 (PSD-95), the major scaffold protein at excitatory synapses, plays a major role in mediating intracellular signaling by synaptic N-methyl-D-aspartate (NMDA) type glutamate receptors. Despite the fact that much is known about the role of PSD-95 in NMDA-mediated toxicity, less is known about its role in mechanical injury, and more specifically, in traumatic brain injury. Given that neural circuitry is disrupted after TBI and that PSD-95 and its interactors end-binding protein 3 (EB3) and adenomatous polyposis coli (APC) shape dendrites, we examined whether changes to these proteins and their interactions occur after brain trauma...
February 12, 2019: Journal of Neurotrauma
Concepció Marin, Cristobal Langdon, Isam Alobid, Mireya Fuentes, Mercè Bonastre, Joaquim Mullol
Excitotoxicity consists in a cascade of intracellular events initiated by an excessive release of glutamate and hyperactivation of glutamatergic receptors that is involved in several pathologies, including traumatic brain injury and neurodegenerative diseases such as Parkinson's disease. Both disorders are a common cause of olfactory dysfunction. We previously reported a role for glutamate excitotoxicity in olfactory dysfunction showing an olfactory deficit 1 week after lesion and a spontaneous recovery 2 weeks after excitotoxicity lesion of the olfactory bulbs (OBs)...
January 19, 2019: Molecular Neurobiology
Elizabeth Ann Fucich, Jacques Pierre Mayeux, M Adrienne McGinn, Nicholas Warren Gilpin, Scott Edwards, Patricia Molina
Traumatic brain injury (TBI) is associated with psychiatric dysfunction-including pain, cognitive impairment, anxiety, and increased alcohol use. We previously demonstrated that inhibiting endocannabinoid degradation post-TBI with JZL184 attenuates neuroinflammation and neuronal hyperexcitability at the site of injury and improves neurobehavioral recovery. This study aimed to determine the effect of JZL184 on post-TBI behavioral changes related to psychiatric dysfunction and post-TBI neuroadaptations in brain regions associated with these behaviors...
January 14, 2019: Journal of Neurotrauma
Joel Tehse, Changiz Taghibiglou
Traumatic brain injury (TBI) is a leading major cause of morbidity and mortality in youth and individuals under 45 year age. A wide variety of cellular and molecular mechanisms have been identified contributing to the pathogenesis of TBI. A better understanding of the pathophysiology behind TBI is essential for providing more effective treatment. Excitotoxicity as one of the secondary molecular events is a major contributing factor in apoptosis and neuronal death following the initial injury in TBI. Excitotoxicity is the rapid overload and influx of calcium into the cell cytoplasm, activating a series of deleterious signaling cascades causing the cell to undergo apoptosis...
December 16, 2018: European Journal of Neuroscience
Xiao-Xuan Fan, Yu-Ying Hao, Shi-Wen Guo, Xiao-Ping Zhao, Yi Xiang, Fei-Xue Feng, Ge-Ting Liang, Yu-Wei Dong
Reticulons (RTNs) are a family of membrane-bound proteins that are dominantly localized to the endoplasmic reticulum (ER) membrane. RTN1-C is one member of RTNs abundantly expressed in the brain and has been shown to mediate neuronal injury in cerebral ischemia models. In the present study, we investigated the role of RTN1-C in an in vitro brain trauma model mimicked by traumatic neuronal injury (TNI) in primary cultured cortical neurons. TNI increased the expression of RTN1-C in cortical neurons but had no effect on RTN1-A and RTN1-B...
October 21, 2018: Neurochemistry International
Péter Hertelendy, Dániel P Varga, Ákos Menyhárt, Ferenc Bari, Eszter Farkas
Secondary injury following acute brain insults significantly contributes to poorer neurological outcome. The spontaneous, recurrent occurrence of spreading depolarization events (SD) has been recognized as a potent secondary injury mechanism in subarachnoid hemorrhage, malignant ischemic stroke and traumatic brain injury. In addition, SD is the underlying mechanism of the aura symptoms of migraineurs. The susceptibility of the nervous tissue to SD is subject to the metabolic status of the tissue, the ionic composition of the extracellular space, and the functional status of ion pumps, voltage-gated and other cation channels, glutamate receptors and excitatory amino acid transporters...
October 15, 2018: Neurochemistry International
Dainan Zhang, Meng Xiao, Long Wang, Wang Jia
Excessive glutamate release has been implicated as a major contributor to multiple post-traumatic brain injury (TBI) deficits, including neurodegeneration and cognitive impairment. Prior to the presence of behavior change, synaptic plasticity is rapidly and potently disrupted by TBI, which is believed to be relevant to inappropriately increased extracellular glutamate concentration and glutamatergic receptor activation. Acutely promoting brain glutamate clearance with a blood-based scavenging system, glutamate oxaloacetate transaminase (GOT), prevents the delayed inhibition of LTP post-TBI...
September 25, 2018: Neurotoxicity Research
Sajad Fakhri, Leila Dargahi, Fatemeh Abbaszadeh, Masoumeh Jorjani
Spinal cord injury (SCI) is a debilitating condition in which inflammatory responses in the secondary phase of injury leads to long lasting sensory-motor dysfunction. The medicinal therapy of SCI complications is still a clinical challenge. Understanding the molecular pathways underlying the progress of damage will help to find new therapeutic candidates. Astaxanthin (AST) is a ketocarotenoid which has shown anti-inflammatory effects in models of traumatic brain injury. In the present study, we examined its potential in the elimination of SCI damage through glutamatergic-phospo p38 mitogen-activated protein kinase (p-p38MAPK) signaling pathway...
September 19, 2018: Brain Research Bulletin
Georgina Perez-Garcia, Miguel A Gama Sosa, Rita De Gasperi, Anna E Tschiffely, Richard M McCarron, Patrick R Hof, Sam Gandy, Stephen T Ahlers, Gregory A Elder
A striking observation among veterans returning from the recent conflicts in Iraq and Afghanistan has been the co-occurrence of blast-related mild traumatic brain injury (mTBI) and post-traumatic stress disorder (PTSD). PTSD and mTBI might coexist due to additive effects of independent psychological and physical traumas experienced in a war zone. Alternatively blast injury might induce PTSD-related traits or damage brain structures that mediate responses to psychological stressors, increasing the likelihood that PTSD will develop following a subsequent psychological stressor...
September 15, 2018: Neuropharmacology
Charles-Francois V Latchoumane, LaDonya Jackson, Mohammad S Eslampanah Sendi, Kayvan F Tehrani, Luke J Mortensen, Steven L Stice, Maysam Ghovanloo, Lohitash Karumbaiah
Functional electrical stimulation (FES) is rapidly gaining traction as a therapeutic tool for mediating the repair and recovery of the injured central nervous system (CNS). However, the underlying mechanisms and impact of these stimulation paradigms at a molecular, cellular and network level remain largely unknown. In this study, we used embryonic stem cell (ESC)-derived neuron and glial co-cultures to investigate network maturation following acute administration of L-glutamate, which is a known mediator of excitotoxicity following CNS injury...
July 19, 2018: Scientific Reports
Nidhi Khatri, Manisha Thankur, Vikas Pareek, Sandeep Kumar, Sunil Sharma, Ashok Kumar Datusalia
Traumatic Brain Injury, representing mild, moderate and severe effects of physical impact on the brain is the leading cause of mortality and morbidity worldwide. Traumatic injury causes sequential, primary and secondary injuries of brain where primary injury is due to the first physical impact, the blow or jolt to the brain compartment. Secondary injury follows primary injury temporally, involving the biochemical, cellular, and physiological responses like blood brain barrier disruption, inflammation, excitotoxicity, necrosis, apoptosis, mitochondrial dysfunction and oxidative stress...
June 27, 2018: CNS & Neurological Disorders Drug Targets
Maja Jazvinšćak Jembrek, Vedrana Radovanović, Josipa Vlainić, Lidija Vuković, Nikolina Hanžić
Excitotoxicity is a pathological process in which neuronal dysfunction and death are induced by excessive glutamate stimulation, the major fast excitatory neurotransmitter in the mammalian brain. Excitotoxicity-induced neurodegeneration is a contributing factor in ischemia-induced brain damage, traumatic brain injury, and various neurodegenerative diseases. It is triggered by calcium overload due to prolonged over-activation of ionotropic N-methyl-d-aspartate (NMDA) receptors. Enhanced Ca2+ release results in neuronal vulnerability through several intertwined mechanisms, including activation of proteolytic enzymes, increased production of reactive oxygen species (ROS), mitochondrial dysfunction and modulation of intracellular signalling pathways...
August 1, 2018: Toxicology
Yutaka Hoshi, Kohki Okabe, Koji Shibasaki, Takashi Funatsu, Norio Matsuki, Yuji Ikegaya, Ryuta Koyama
Brain edema is characterized by an increase in net brain water content, which results in an increase in brain volume. Although brain edema is associated with a high fatality rate, the cellular and molecular processes of edema remain largely unclear. Here, we developed an in vitro model of ischemic stroke-induced edema in which male mouse brain slices were treated with oxygen-glucose deprivation (OGD) to mimic ischemia. We continuously measured the cross-sectional area of the brain slice for 150 min under macroscopic microscopy, finding that OGD induces swelling of brain slices...
June 20, 2018: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Garik V Mkrtchyan, Muammer Üçal, Andrea Müllebner, Sergiu Dumitrescu, Martina Kames, Rudolf Moldzio, Marek Molcanyi, Samuel Schaefer, Adelheid Weidinger, Ute Schaefer, Juergen Hescheler, Johanna Catharina Duvigneau, Heinz Redl, Victoria I Bunik, Andrey V Kozlov
BACKGROUND AND PURPOSE: Based on the fact that traumatic brain injury is associated with mitochondrial dysfunction we aimed at localization of mitochondrial defect and attempted to correct it by thiamine. EXPERIMENTAL APPROACH: Interventional controlled experimental animal study was used. Adult male Sprague-Dawley rats were subjected to lateral fluid percussion traumatic brain injury. Thiamine was administered 1 h prior to trauma; cortex was extracted for analysis 4 h and 3 d after trauma...
September 2018: Biochimica et biophysica acta. Bioenergetics
Austin J Peters, Laura E Villasana, Eric Schnell
WHAT WE ALREADY KNOW ABOUT THIS TOPIC: WHAT THIS ARTICLE TELLS US THAT IS NEW: BACKGROUND:: Traumatic brain injury induces cellular proliferation in the hippocampus, which generates new neurons and glial cells during recovery. This process is regulated by N-methyl-D-aspartate-type glutamate receptors, which are inhibited by ketamine. The authors hypothesized that ketamine treatment after traumatic brain injury would reduce hippocampal cell proliferation, leading to worse behavioral outcomes in mice...
August 2018: Anesthesiology
Wei Bai, Ping Li, Ya-Lei Ning, Yu-Lin Jiang, Nan Yang, Xing Chen, Yuan-Guo Zhou
Traumatic brain injury-induced acute lung injury (TBI-ALI) is a serious complication of traumatic brain injury (TBI). Our previous clinical study found that high levels of blood glutamate after TBI were closely related to the occurrence and severity of TBI-ALI, while it remains unknown whether a high concentration of blood glutamate directly causes or aggravates TBI-ALI. We found that inhibition of the adenosine A2A receptor (A2AR) after brain injury alleviated the TBI-ALI; however, it is unknown whether lowering blood glutamate levels in combination with inhibiting the A2AR would lead to better effects...
April 23, 2018: Shock
Sigal Liraz-Zaltsman, Barbara Slusher, Dana Atrakchi-Baranes, Kineret Rosenblatt, Yael Friedman Levi, Efrat Kesner, Alcino J Silva, Anat Biegon, Esther Shohami
Cognitive deficits, especially memory loss, are common and devastating neuropsychiatric sequelae of traumatic brain injury (TBI). The deficits may persist for years and may be accompanied by increased risk of developing early- onset dementia. Past attempts to reverse the neuropathological effects of brain injury with glutamate-N-methyl-d-aspartate (NMDA) antagonists failed to show any benefits or worsened the outcome, suggesting that activation, rather than blockage, of the NMDA receptor (NMDAR) may be useful in the subacute period after TBI and stroke...
July 15, 2018: Journal of Neurotrauma
Wei Bai, Ping Li, Ya-Lei Ning, Yan Peng, Ren-Ping Xiong, Nan Yang, Xing Chen, Yuan-Guo Zhou
Excitatory amino acid transporters (EAATs) on cerebral vascular endothelial cells play an important role in maintaining glutamate homeostasis in the brain. The dysfunction of endothelial EAATs is an important reason for the dramatically elevated brain glutamate levels after brain injury, such as traumatic brain injury (TBI). The adenosine A2A receptor (A2A R) plays an important role in regulating the brain glutamate level after brain injury; however, researchers have not clearly determined whether this role was related to its ability to regulate endothelial EAATs...
April 15, 2018: Biochemical and Biophysical Research Communications
Georgina Perez-Garcia, Rita De Gasperi, Miguel A Gama Sosa, Gissel M Perez, Alena Otero-Pagan, Anna Tschiffely, Richard M McCarron, Stephen T Ahlers, Gregory A Elder, Sam Gandy
Battlefield blast exposure related to improvised explosive devices (IEDs) has become the most common cause of traumatic brain injury (TBI) in the recent conflicts in Iraq and Afghanistan. Mental health problems are common after TBI. A striking feature in the most recent veterans has been the frequency with which mild TBI (mTBI) and posttraumatic stress disorder (PTSD) have appeared together, in contrast to the classical situations in which the presence of mTBI has excluded the diagnosis of PTSD. However, treatment of PTSD-related symptoms that follow blast injury has become a significant problem...
January 2018: ENeuro
Che-Chuan Wang, Hsiao-Yue Wee, Chiao-Ya Hu, Chung-Ching Chio, Jinn-Rung Kuo
BACKGROUND: The main aim of this study is to elucidate whether the neuroprotective effect of memantine, a noncompetitive N-methyl-d-aspartate receptor 2B (NR2B) antagonist, affects neuronal nitrosative stress, apoptosis, and NR2B expression and improves functional outcomes. METHODS: Immediately after the onset of fluid percussion traumatic brain injury (TBI), anesthetized male Sprague-Dawley rats were divided into sham-operated, TBI + vehicle, and TBI + memantine groups...
April 2018: World Neurosurgery
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