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Excitotoxicity

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https://www.readbyqxmd.com/read/28087338/auditory-hindbrain-atrophy-and-anomalous-calcium-binding-protein-expression-after-neonatal-exposure-to-monosodium-glutamate
#1
Lindsey Foran, Kaitlyn Blackburn, Randy J Kulesza
Glutamate is the most abundant excitatory neurotransmitter in the central nervous system, and is stored and released by both neurons and astrocytes. Despite the important role of glutamate as a neurotransmitter, elevated extracellular glutamate can result in excitotoxicity and apoptosis. Monosodium glutamate (MSG) is a naturally occurring sodium salt of glutamic acid that is used as a flavor enhancer in many processed foods. Previous studies have shown that MSG administration during the early postnatal period results in neurodegenerative changes in several forebrain regions, characterized by neuronal loss and neuroendocrine abnormalities...
January 10, 2017: Neuroscience
https://www.readbyqxmd.com/read/28087150/apelin-protects-against-nmda-induced-retinal-neuronal-death-via-an-apj-receptor-by-activating-akt-and-erk1-2-and-suppressing-tnf-%C3%AE-expression-in-mice
#2
Yuki Ishimaru, Akihide Sumino, Daiki Kajioka, Fumiya Shibagaki, Akiko Yamamuro, Yasuhiro Yoshioka, Sadaaki Maeda
Glutamate excitotoxicity mediated by N-methyl-d-aspartate (NMDA) receptors is an important cause of retinal ganglion cell death in glaucoma. To elucidate whether apelin protects against retinal neuronal cell death, we examined protective effects of exogenous and endogenous apelin on neuronal cell death induced by intravitreal injection of NMDA in the retinas of mice. An intravitreal injection of NMDA induced neuronal cell death in both the retinal ganglion cell layer and inner nuclear layer, and reduced the amplitudes of scotopic threshold response (STR) in electroretinography studies...
December 24, 2016: Journal of Pharmacological Sciences
https://www.readbyqxmd.com/read/28086920/absence-of-system-xc-on-immune-cells-invading-the-central-nervous-system-alleviates-experimental-autoimmune-encephalitis
#3
Ellen Merckx, Giulia Albertini, Magdalena Paterka, Cathy Jensen, Philipp Albrecht, Michael Dietrich, Joeri Van Liefferinge, Eduard Bentea, Lise Verbruggen, Thomas Demuyser, Lauren Deneyer, Jan Lewerenz, Geert van Loo, Jacques De Keyser, Hideyo Sato, Pamela Maher, Axel Methner, Ann Massie
BACKGROUND: Multiple sclerosis (MS) is an autoimmune demyelinating disease that affects the central nervous system (CNS), leading to neurodegeneration and chronic disability. Accumulating evidence points to a key role for neuroinflammation, oxidative stress, and excitotoxicity in this degenerative process. System xc(-) or the cystine/glutamate antiporter could tie these pathological mechanisms together: its activity is enhanced by reactive oxygen species and inflammatory stimuli, and its enhancement might lead to the release of toxic amounts of glutamate, thereby triggering excitotoxicity and neurodegeneration...
January 13, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28079589/in-vogue-ketamine-for-neuroprotection-in-acute-neurologic-injury
#4
Josh D Bell
Neurologic deterioration following acute injury to the central nervous system may be amenable to pharmacologic intervention, although, to date, no such therapy exists. Ketamine is an anesthetic and analgesic emerging as a novel therapy for a number of clinical entities in recent years, including refractory pain, depression, and drug-induced hyperalgesia due to newly discovered mechanisms of action and new application of its known pharmacodynamics. In this focused review, the evidence for ketamine as a neuroprotective agent in stroke, neurotrauma, subarachnoid hemorrhage, and status epilepticus is highlighted, with a focus on its applications for excitotoxicity, neuroinflammation, and neuronal hyperexcitability...
January 10, 2017: Anesthesia and Analgesia
https://www.readbyqxmd.com/read/28079313/postischemic-inflammation-in-acute-stroke
#5
REVIEW
Simone Vidale, Arturo Consoli, Marco Arnaboldi, Domenico Consoli
Cerebral ischemia is caused by arterial occlusion due to a thrombus or an embolus. Such occlusion induces multiple and concomitant pathophysiological processes that involve bioenergetic failure, acidosis, loss of cell homeostasis, excitotoxicity, and disruption of the blood-brain barrier. All of these mechanisms contribute to neuronal death, mainly via apoptosis or necrosis. The immune system is involved in this process in the early phases after brain injury, which contributes to potential enlargement of the infarct size and involves the penumbra area...
January 2017: Journal of Clinical Neurology
https://www.readbyqxmd.com/read/28078987/role-of-proinflammatory-cytokines-in-dopaminergic-system-disturbances-implications-for-anhedonic-features-of-mdd
#6
Zihang Pan, Joshua D Rosenblat, Walter Swardfager, Roger S McIntyre
Anhedonia, characterized by a loss of interest and/or pleasure in previously enjoyable activities, is an important diagnostic criterion of Major Depressive Disorder (MDD). Converging evidence implicates a behaviouralcausal relationship between proinflammatory cytokines and disturbances that characterize anhedonia in the context of MDD. Additionally, anhedonia has been implicated in disturbances of key central dopaminergic modulatory pathways. Emerging research into the roles of tetrahydrobiopterin, a cytokine-targeted co-enzyme in the synthesis of dopamine, and kynurenine, a product of inflammation-sensitive breakdown of tryptophan via indoleamine 2, 3-dioxygenase, have shed new light into the role of inflammation in mediating anhedonic behaviours...
January 11, 2017: Current Pharmaceutical Design
https://www.readbyqxmd.com/read/28073324/3-methoxy-aroylhydrazones-free-radicals-scavenging-anticancer-and-cytoprotective-potency
#7
Nadya Hristova-Avakumova, Krassimira Yoncheva, Boryana Nikolova-Mladenova, Trayko Traykov, Georgi Momekov, Vera Hadjimitova
OBJECTIVE: This study aimed to determine the capability of newly designed 3-methoxy derivatives of salicylaldehyde benzoylhydrazone to influence the oxidative stress processes and to test their in vitro cytotoxicity. METHODS: We have used chemiluminescent and spectrophotometric model systems containing different types of reactive oxygen species (OH(●), OCl(─) and O2(─●)). The hydrazones effect on the viability of Hep-G2, HEK-293 and SH-SY5Y cell lines was determined via MTT assay...
January 10, 2017: Redox Report: Communications in Free Radical Research
https://www.readbyqxmd.com/read/28068984/effect-of-tualang-honey-against-ka-induced-oxidative-stress-and-neurodegeneration-in-the-cortex-of-rats
#8
Nur Shafika Mohd Sairazi, Sirajudeen K N S, Mohd Asnizam Asari, Swamy Mummedy, Mustapha Muzaimi, Siti Amrah Sulaiman
BACKGROUND: Administration of KA on rodents has resulted in seizures, behavioral changes, oxidative stress, and neuronal degeneration on selective population of neurons in the brain. The present study was undertaken to investigate the extent of neuroprotective effect conferred by Malaysian Tualang Honey (TH), an antioxidant agent, in the cerebral cortex of rats against KA-induced oxidative stress and neurodegeneration in an animal model of KA-induced excitotoxicity. METHODS: Male Sprague-Dawley rats were randomly divided into five groups: Control, KA-treated group, TH + KA-treated group, aspirin (ASP; anti-inflammatory agent) + KA-treated group and topiramate (TPM; antiepileptic agent) + KA-treated group...
January 9, 2017: BMC Complementary and Alternative Medicine
https://www.readbyqxmd.com/read/28065841/the-neurotoxic-mechanisms-of-amphetamine-step-by-step-for-striatal-dopamine-depletion
#9
Che-Se Tung, Shang-Tang Chang, Chuen-Lin Huang, Nai-Kuei Huang
Amphetamine (AMPH) is a commonly abused psychostimulant that induces neuronal cell death/degeneration in humans and experimental animals. Although multiple neurotoxic mechanisms of AMPH have been intensively investigated, the interplay between these mechanisms has remained elusive. In this study, we used a rat model of AMPH-induced long-lasting striatal dopamine (DA) depletion and identified mechanisms of neurotoxicity, energy failure, excitotoxicity, and oxidative stress. Pretreatment with nicotinamide (NAM, a co-factor for the electron transport chain) blocked AMPH-induced free radical formation, energy failure, and striatal DA decrease...
January 6, 2017: Neuroscience Letters
https://www.readbyqxmd.com/read/28065796/ischaemia-and-excitotoxicity-induced-camkii-mediated-neuronal-cell-death-the-relative-roles-of-camkii-autophosphorylation-at-t286-and-t253
#10
John A P Rostas, Alexander Hoffman, Lucy A Murtha, Debbie Pepperall, Damian D McLeod, Phillip W Dickson, Neil J Spratt, Kathryn A Skelding
Ischaemia/excitotoxicity produces persistent activation of CaMKII (Ca(2+)-calmodulin stimulated protein kinase II) that initiates cell death. This study investigated the involvement of CaMKII phosphorylation at T286 and T253 in producing this persistent activation. In T286A-αCaMKII transgenic mice that lack the ability to phosphorylate αCaMKII at T286, transient occlusion of the middle cerebral artery for 90 min resulted in no significant difference in infarct size compared to normal littermate controls...
January 5, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28065781/ischemic-brain-injury-new-insights-on-the-protective-role-of-melatonin
#11
REVIEW
Eva Ramos, Paloma Patiño, Russel J Reiter, Emilio Gil-Martín, José Marco-Contelles, Esther Parada, Cristobal de Los Rios, Alejandro Romero, Javier Egea
Stroke represents one of the most common causes of brain's vulnerability for many millions of people worldwide. The plethora of physiopathological events associated with brain ischemia are regulate through multiple signaling pathways leading to the activation of oxidative stress process, Ca(2+) dyshomeostasis, mitochondrial dysfunction, proinflammatory mediators, excitotoxicity and/or programmed neuronal cell death. Understanding this cascade of molecular events is mandatory in order to develop new therapeutic strategies for stroke...
January 6, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28063880/glur3b-ab-s-induced-oligodendrocyte-precursor-cells-excitotoxicity-via-mitochondrial-dysfunction
#12
Yi Liu, Yan Chen, Wan Tong Du, Xiu Xiang Wu, Fu Xing Dong, Xue Bin Qu, Hong Bin Fan, Rui Qin Yao
Studies have indicated that glutamate receptor subunit 3 peptide B antibodies (GluR3B Ab's) by directing against a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid subtype glutamate receptors (AMPARs) subunit 3 (GluR3B) was involved in the hippocampal neuron damage in the pathogenesis of epilepsy. Glutamate accumulation is critical for oligodendrocyte precursors (OPCs) excitotoxic injury. However, remarkably little is known about whether GluR3B Ab's causes OPCs excitotoxicity, and the underlying mechanisms remain unclear...
January 4, 2017: Brain Research Bulletin
https://www.readbyqxmd.com/read/28050710/the-copper-bis-thiosemicarbazone-complex-cu-ii-atsm-is-protective-against-cerebral-ischemia-through-modulation-of-the-inflammatory-milieu
#13
Mikko T Huuskonen, Qing-Zhang Tuo, Sanna Loppi, Hiramani Dhungana, Paula Korhonen, Lachlan E McInnes, Paul S Donnelly, Alexandra Grubman, Sara Wojciechowski, Katarina Lejavova, Yuriy Pomeshchik, Laura Periviita, Lotta Kosonen, Martina Giordano, Frederick R Walker, Rong Liu, Ashley I Bush, Jari Koistinaho, Tarja Malm, Anthony R White, Peng Lei, Katja M Kanninen
Developing new therapies for stroke is urgently needed, as this disease is the leading cause of death and disability worldwide, and the existing treatment is only available for a small subset of patients. The interruption of blood flow to the brain during ischemic stroke launches multiple immune responses, characterized by infiltration of peripheral immune cells, the activation of brain microglial cells, and the accumulation of immune mediators. Copper is an essential trace element that is required for many critical processes in the brain...
January 3, 2017: Neurotherapeutics: the Journal of the American Society for Experimental NeuroTherapeutics
https://www.readbyqxmd.com/read/28049198/mechanism-of-2-3-4-5-tetrahydroxystilbene-2-o-%C3%AE-d-glucoside-induced-upregulation-of-glutamate-transporter-1-protein-expression-in-mouse-primary-astrocytes
#14
Xiangfan Chen, Wenfeng Hu, Xu Lu, Bo Jiang, Jili Wang, Wei Zhang, Chao Huang
Glutamate transporter-1 (GLT-1), a major glutamate transporter expressed in astrocytes, takes up excess glutamate from the micro-environment in order to prevent excitotoxicity. Drugs that increase GLT-1 expression may have therapeutic effects in disorders associated with neuronal excitotoxicity. 2,3,4',5-tetrahydroxystilbene 2-O-β-D-glucoside (TSG), a monomer of stilbene from polygonummultiflorum, exerts neuroprotection in a range of experimental models such as Alzheimer's disease and brain ischemia. In this study, we evaluated the effect of TSG on GLT-1 protein expression in mouse primary-cultured astrocytes...
January 4, 2017: Pharmacology
https://www.readbyqxmd.com/read/28045138/tfp5-peptide-derived-from-cdk5-activating-cofactor-p35-provides-neuroprotection-in-early-stage-of-adult-ischemic-stroke
#15
Ya-Bin Ji, Pei-Pei Zhuang, Zhong Ji, Yong-Ming Wu, Yong Gu, Xiao-Ya Gao, Su-Yue Pan, Ya-Fang Hu
Cyclin-dependent kinase 5 (CDK5) is a multifaceted protein shown to play important roles in the central nervous system. Abundant evidence indicates that CDK5 hyperactivities associated with neuronal apoptosis and death following ischemic stroke. CDK5 activity increases when its cofactor p35 cleaves into p25 during ischemia. Theoretically, inhibition of CDK5/p25 activity or reduction of p25 would be neuroprotective. TFP5, a modified 24-aa peptide (Lys254-Ala277) derived from p35, was found to effectively inhibit CDK5 hyperactivity and improve the outcomes of Alzheimer's disease and Parkinson's disease in vivo...
January 3, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28045134/methamphetamine-and-ovarian-steroid-responsive-cells-in-the-posteriodorsal-medial-amygdala-are-required-for-methamphetamine-enhanced-proceptive-behaviors
#16
Katrina M Williams, Jessica A Mong
Methamphetamine (Meth) is a psychomotor stimulant strongly associated with increases in sexual drive and impulse in both men and women. These changes in sexual motivation have a greater impact on women due to their likelihood of facing the greater burden of unplanned pregnancies, as well as increased risk for psychiatric co-morbidities such as depression. We have previously established a rodent model of Meth-induced increases in sexual motivation. Using this model, we have identified the posteriodorsal medial amygdala (MePD) via excitotoxic lesion studies as a necessary nucleus in Meth-facilitated female sexual motivation...
January 3, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28040508/molecular-and-cellular-physiology-of-sodium-dependent-glutamate-transporters
#17
Christine R Rose, Daniel Ziemens, Verena Untiet, Christoph Fahlke
Glutamate is the major excitatory transmitter in the vertebrate brain. After its release from presynaptic nerve terminals, it is rapidly taken up by high-affinity sodium-dependent plasma membrane transporters. While both neurons and glial cells express these excitatory amino acid transporters (EAATs), the majority of glutamate uptake is accomplished by astrocytes, which convert synaptically-released glutamate to glutamine or feed it into their own metabolism. Glutamate uptake by astrocytes not only shapes synaptic transmission by regulating the availability of glutamate to postsynaptic neuronal receptors, but also protects neurons from hyper-excitability and subsequent excitotoxic damage...
December 28, 2016: Brain Research Bulletin
https://www.readbyqxmd.com/read/28039593/early-and-late-pathomechanisms-in-alzheimer-s-disease-from-zinc-to-amyloid-%C3%AE-neurotoxicity
#18
Andrzej Szutowicz, Hanna Bielarczyk, Marlena Zyśk, Aleksandra Dyś, Anna Ronowska, Sylwia Gul-Hinc, Joanna Klimaszewska-Łata
There are several systemic and intracerebral pathologic conditions, which limit provision and utilization of energy precursor metabolites in neuronal cells. Energy deficits cause excessive depolarization of neuronal cells triggering glutamate-zinc evoked excitotoxic cascade. The intracellular zinc excess hits several intraneuronal targets yielding collapse of energy balance and impairment functional and structural impairments cholinergic neurons. Disturbances in metabolism of acetyl-CoA, which is a direct precursor for energy, acetylcholine, N-acetyl-L-aspartate and acetylated proteins synthesis, play an important role in these pathomechanisms...
December 30, 2016: Neurochemical Research
https://www.readbyqxmd.com/read/28028152/pharmacologic-inhibition-of-hsp90-to-prevent-glt-1-degradation-as-an-effective-therapy-for-epilepsy
#19
Longze Sha, Xueqin Wang, Jing Li, Xinze Shi, Liwen Wu, Yan Shen, Qi Xu
The glutamate transporter GLT-1 is critical for the maintenance of low interstitial glutamate concentrations. Loss of GLT-1 is commonly observed in neurological disorders, including temporal lobe epilepsy (TLE). Despite the hypothesis that targeting the mechanisms of GLT-1 deficiency may be a novel strategy for treating drug-resistant epilepsy, the underlying molecular cascade remains largely unknown. Here, we show that Hsp90β is up-regulated in reactive astrocytes of the epileptic hippocampus in patients with TLE and mouse models of epilepsy...
December 27, 2016: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/28027448/induced-pluripotent-hd-monkey-stem-cells-derived-neural-cells-for-drug-discovery
#20
Tanut Kunkanjanawan, Richard Carter, Kwan-Sung Ahn, Jinjing Yang, Rangsun Parnpai, Anthony W S Chan
Huntington's disease (HD) is a neurodegenerative disease caused by an expansion of CAG trinucleotide repeat (polyglutamine [polyQ]) in the huntingtin ( HTT) gene, which leads to the formation of mutant HTT (mHTT) protein aggregates. In the nervous system, an accumulation of mHTT protein results in glutamate-mediated excitotoxicity, proteosome instability, and apoptosis. Although HD pathogenesis has been extensively studied, effective treatment of HD has yet to be developed. Therapeutic discovery research in HD has been reported using yeast, cells derived from transgenic animal models and HD patients, and induced pluripotent stem cells from patients...
December 1, 2016: Journal of Biomolecular Screening
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