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Excitotoxicity

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https://www.readbyqxmd.com/read/28230232/carisbamate-blockade-of-t-type-voltage-gated-calcium-channels
#1
Do Young Kim, Fang-Xiong Zhang, Stan T Nakanishi, Timothy Mettler, Ik-Hyun Cho, Younghee Ahn, Florian Hiess, Lina Chen, Patrick G Sullivan, S R Wayne Chen, Gerald W Zamponi, Jong M Rho
OBJECTIVES: Carisbamate (CRS) is a novel monocarbamate compound that possesses antiseizure and neuroprotective properties. However, the mechanisms underlying these actions remain unclear. Here, we tested both direct and indirect effects of CRS on several cellular systems that regulate intracellular calcium concentration [Ca(2+) ]i . METHODS: We used a combination of cellular electrophysiologic techniques, as well as cell viability, Store Overload-Induced Calcium Release (SOICR), and mitochondrial functional assays to determine whether CRS might affect [Ca(2+) ]i levels through actions on the endoplasmic reticulum (ER), mitochondria, and/or T-type voltage-gated Ca(2+) channels...
February 23, 2017: Epilepsia
https://www.readbyqxmd.com/read/28229936/neurons-of-the-rat-cervical-spinal-cord-express-vimentin-and-neurofilament-after-intraparenchymal-injection-of-kainic-acid
#2
Fabián Nishida, Susana M Sisti, Carolina N Zanuzzi, Claudio G Barbeito, Enrique L Portiansky
Intermediate filaments (IF) can be altered under disorders such as neurodegenerative diseases. Kainic acid (KA) induce behavioral changes and histopathological alterations of the spinal cord of injected rats. Our goal was to evaluate the IF expression in neurons during this injury model. Animals were injected with KA at the C5 segment of the cervical spinal cord and euthanized at 1, 3 and 7 post injection (pi) days. Neuronal cell counting showed a significant loss of neurons at the injection site when compared with those of sham and non-operated animals...
February 13, 2017: Neuroscience Letters
https://www.readbyqxmd.com/read/28226865/electrical-resistance-increases-at-the-tissue-electrode-interface-as-an-early-response-to-nucleus-accumbens-deep-brain-stimulation
#3
Rajas P Kale, Abbas Z Kouzani, Julian Berk, Ken Walder, Michael Berk, Susannah J Tye, Rajas P Kale, Abbas Z Kouzani, Julian Berk, Ken Walder, Michael Berk, Susannah J Tye, Julian Berk, Michael Berk, Susannah J Tye, Abbas Z Kouzani, Rajas P Kale, Ken Walder
The therapeutic actions of deep brain stimulation are not fully understood. The early inflammatory response of electrode implantation is associated with symptom relief without electrical stimulation, but is negated by anti-inflammatory drugs. Early excitotoxic necrosis and subsequent glial scarring modulate the conductivity of the tissue-electrode interface, which can provide some detail into the inflammatory response of individual patients. The feasibility of this was demonstrated by measuring resistance values across a bipolar electrode which was unilaterally implanted into the nucleus accumbens of a rat while receiving continuous deep brain stimulation with a portable back-mounted device using clinical parameters (130Hz, 200μA, 90μs) for 3 days...
August 2016: Conference Proceedings: Annual International Conference of the IEEE Engineering in Medicine and Biology Society
https://www.readbyqxmd.com/read/28222432/extracellular-hmgb1-modulates-glutamate-metabolism-associated-with-kainic-acid-induced-epilepsy-like-hyperactivity-in-primary-rat-neural-cells
#4
Yuji Kaneko, Colleen Pappas, Teresita Malapira, Fernando Ĺ Vale, Naoki Tajiri, Cesar V Borlongan
BACKGROUND/AIMS: Neuroinflammatory processes have been implicated in the pathophysiology of seizure/epilepsy. High mobility group box 1 (HMGB1), a non-histone DNA binding protein, behaves like an inflammatory cytokine in response to epileptogenic insults. Kainic acid (KA) is an excitotoxic reagent commonly used to induce epilepsy in rodents. However, the molecular mechanism by which KA-induced HMGB1 affords the initiation of epilepsy, especially the role of extracellular HMGB1 in neurotransmitter expression, remains to be elucidated...
February 20, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/28220060/a-pulsed-electromagnetic-field-protects-against-glutamate-induced-excitotoxicity-by-modulating-the-endocannabinoid-system-in-ht22-cells
#5
Xin Li, Haoxiang Xu, Tao Lei, Yuefan Yang, Da Jing, Shuhui Dai, Peng Luo, Qiaoling Xu
Glutamate-induced excitotoxicity is common in the pathogenesis of many neurological diseases. A pulsed electromagnetic field (PEMF) exerts therapeutic effects on the nervous system, but its specific mechanism associated with excitotoxicity is still unknown. We investigated the role of PEMF exposure in regulating glutamate-induced excitotoxicity through the endocannabinoid (eCB) system. PEMF exposure improved viability of HT22 cells after excitotoxicity and reduced lactate dehydrogenase release and cell death...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28217291/paradigms-and-mechanisms-of-inhalational-anesthetics-mediated-neuroprotection-against-cerebral-ischemic-stroke
#6
REVIEW
Hailian Wang, Peiying Li, Na Xu, Ling Zhu, Mengfei Cai, Weifeng Yu, Yanqin Gao
Cerebral ischemic stroke is a leading cause of serious long-term disability and cognitive dysfunction. The high mortality and disability of cerebral ischemic stroke is urging the health providers, including anesthesiologists and other perioperative professioners, to seek effective protective strategies, which are extremely limited, especially for those perioperative patients. Intriguingly, several commonly used inhalational anesthetics are recently suggested to possess neuroprotective effects against cerebral ischemia...
October 2016: Medical Gas Research
https://www.readbyqxmd.com/read/28217084/nad-attenuates-bilirubin-induced-hyperexcitation-in-the-ventral-cochlear-nucleus-by-inhibiting-excitatory-neurotransmission-and-neuronal-excitability
#7
Min Liang, Xin-Lu Yin, Lu-Yang Wang, Wei-Hai Yin, Ning-Ying Song, Hai-Bo Shi, Chun-Yan Li, Shan-Kai Yin
Nicotinamide adenine dinucleotide (NAD+) is an important molecule with extensive biological functions in various cellular processes, including protection against cell injuries. However, little is known regarding the roles of NAD+ in neuronal excitation and excitotoxicity associated with many neurodegenerative disorders and diseases. Using patch-clamp recordings, we studied its potential effects on principal neurons in the ventral cochlear nucleus (VCN), which is particularly vulnerable to bilirubin excitotoxicity...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28210211/app-as-a-protective-factor-in-acute-neuronal-insults
#8
REVIEW
Dimitri Hefter, Andreas Draguhn
Despite its key role in the molecular pathology of Alzheimer's disease (AD), the physiological function of amyloid precursor protein (APP) is unknown. Increasing evidence, however, points towards a neuroprotective role of this membrane protein in situations of metabolic stress. A key observation is the up-regulation of APP following acute (stroke, cardiac arrest) or chronic (cerebrovascular disease) hypoxic-ischemic conditions. While this mechanism may increase the risk or severity of AD, APP by itself or its soluble extracellular fragment APPsα can promote neuronal survival...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28210207/cannabinoid-receptor-2-signaling-in-neurodegenerative-disorders-from-pathogenesis-to-a-promising-therapeutic-target
#9
REVIEW
Tommaso Cassano, Silvio Calcagnini, Lorenzo Pace, Federico De Marco, Adele Romano, Silvana Gaetani
As a consequence of an increasingly aging population, the number of people affected by neurodegenerative disorders, such as Alzheimer's disease, Parkinson's disease and Huntington's disease, is rapidly increasing. Although the etiology of these diseases has not been completely defined, common molecular mechanisms including neuroinflammation, excitotoxicity and mitochondrial dysfunction have been confirmed and can be targeted therapeutically. Moreover, recent studies have shown that endogenous cannabinoid signaling plays a number of modulatory roles throughout the central nervous system (CNS), including the neuroinflammation and neurogenesis...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28208701/excitotoxins-mitochondrial-and-redox-disturbances-in-multiple-sclerosis
#10
REVIEW
Cecilia Rajda, Dániel Pukoli, Zsuzsanna Bende, Zsófia Majláth, László Vécsei
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). There is increasing evidence that MS is not only characterized by immune mediated inflammatory reactions, but also by neurodegenerative processes. There is cumulating evidence that neurodegenerative processes, for example mitochondrial dysfunction, oxidative stress, and glutamate (Glu) excitotoxicity, seem to play an important role in the pathogenesis of MS. The alteration of mitochondrial homeostasis leads to the formation of excitotoxins and redox disturbances...
February 8, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28205585/neuronally-directed-effects-of-rxr-activation-in-a-mouse-model-of-alzheimer-s-disease
#11
M M Mariani, T Malm, R Lamb, T R Jay, L Neilson, B Casali, L Medarametla, G E Landreth
Alzheimer's disease (AD) is characterized by extensive neuron loss that accompanies profound impairments in memory and cognition. We examined the neuronally directed effects of the retinoid X receptor agonist bexarotene in an aggressive model of AD. We report that a two week treatment of 3.5 month old 5XFAD mice with bexarotene resulted in the clearance of intraneuronal amyloid deposits. Importantly, neuronal loss was attenuated by 44% in the subiculum in mice 4 months of age and 18% in layer V of the cortex in mice 8 months of age...
February 16, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28195577/hippocampus-glutamate-and-n-acetyl-aspartate-markers-of-excitotoxic-neuronal-compromise-in-posttraumatic-stress-disorder
#12
Isabelle M Rosso, David J Crowley, Marisa M Silveri, Scott L Rauch, J Eric Jensen
Hippocampus atrophy is implicated in posttraumatic stress disorder (PTSD), and may partly reflect stress-induced glutamate excitotoxicity that culminates in neuron injury and manifests as re-experiencing symptoms and other memory abnormalities. This study used high-field proton magnetic resonance spectroscopy (MRS) to determine whether PTSD is associated with lower hippocampus levels of the neuron marker N-acetyl aspartate (NAA), along with higher levels of glutamate (Glu) and Glu/NAA. We also predicted that metabolite levels would correlate with re-experiencing symptoms and lifetime trauma load...
February 13, 2017: Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology
https://www.readbyqxmd.com/read/28193238/transient-ikk2-activation-in-astrocytes-initiates-selective-non-cell-autonomous-neurodegeneration
#13
Michael Lattke, Stephanie N Reichel, Alexander Magnutzki, Alireza Abaei, Volker Rasche, Paul Walther, Dinis P Calado, Boris Ferger, Thomas Wirth, Bernd Baumann
BACKGROUND: Neuroinflammation is associated with a wide range of neurodegenerative disorders, however the specific contribution to individual disease pathogenesis and selective neuronal cell death is not well understood. Inflammatory cerebellar ataxias are neurodegenerative diseases occurring in various autoimmune/inflammatory conditions, e.g. paraneoplastic syndromes. However, how inflammatory insults can cause selective cerebellar neurodegeneration in the context of these diseases remains open, and appropriate animal models are lacking...
February 13, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28192082/endocannabinoid-dependent-protection-against-kainic-acid-induced-long-term-alteration-of-brain-oscillations-in-guinea-pigs
#14
Liubov Shubina, Rubin Aliev, Valentina Kitchigina
Changes in rhythmic activity can serve as early biomarkers of pathological alterations, but it remains unclear how different types of rhythmic activity are altered during neurodegenerative processes. Glutamatergic neurotoxicity, evoked by kainic acid (KA), causes hyperexcitation and acute seizures that result in delayed brain damage. We employed wide frequency range (0.1-300 Hz) local field potential recordings in guinea pigs to study the oscillatory activity of the hippocampus, entorhinal cortex, medial septum, and amygdala in healthy animals for three months after KA introduction...
February 9, 2017: Brain Research
https://www.readbyqxmd.com/read/28185129/folic-acid-protects-against-glutamate-induced-excitotoxicity-in-hippocampal-slices-through-a-mechanism-that-implicates-inhibition-of-gsk-3%C3%AE-and-inos
#15
Josiane Budni, Simone Molz, Tharine Dal-Cim, Maria Dolores Martín-de-Saavedra, Javier Egea, Manuela G Lopéz, Carla Ines Tasca, Ana Lúcia Severo Rodrigues
Folic acid (folate) is a vitamin of the B-complex group crucial for neurological function. Considering that excitotoxicity and cell death induced by glutamate are involved in many disorders, the potential protective effect of folic acid on glutamate-induced cell damage in rat hippocampal slices and the possible intracellular signaling pathway involved in such effect were investigated. The treatment of hippocampal slices with folic acid (100 μM) significantly abrogated glutamate (1 mM)-induced reduction of cell viability measured by MTT reduction assay and inhibited glutamate-induced D-[(3)H]-aspartate release...
February 10, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28181189/deficit-but-not-nondeficit-schizophrenia-is-characterized-by-mucosa-associated-activation-of-the-tryptophan-catabolite-trycat-pathway-with-highly-specific-increases-in-iga-responses-directed-to-picolinic-xanthurenic-and-quinolinic-acid
#16
Buranee Kanchanatawan, Sunee Sirivichayakul, Kiat Ruxrungtham, André F Carvalho, Michel Geffard, Heidi Ormstad, George Anderson, Michael Maes
Evidence suggests that activation of the tryptophan catabolite (TRYCAT) pathway is involved in the pathophysiology of schizophrenia. However, no previous study examined whether TRYCAT pathway activation is associated with deficit schizophrenia. We measured IgA responses to TRYCATs, namely quinolinic acid, picolinic acid, kynurenic acid, xanthurenic acid, and anthranilic acid and 3-OH-kynurenine, in 40 healthy controls and in schizophrenic patients with (n = 40) and without (n = 40) deficit, defined according to the Schedule for the Deficit Syndrome (SDS)...
February 8, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28174214/excitotoxicity-induced-immediate-prostaglandin-d2-production-induces-sustained-microglial-activation-and-delayed-neuronal-death-in-the-hippocampus
#17
Kensuke Iwasa, Shinji Yamamoto, Sosuke Yagishita, Kei Maruyama, Keisuke Yoshikawa
Excitotoxicity is the pivotal mechanism of neuronal death. Prostaglandins (PGs) produced during excitotoxicity play important roles in neurodegenerative conditions. Previously, we demonstrated that initial burst productions of PGD2, PGE2 and PGF2alpha are produced by Cyclooxygenase-2 (COX-2) in the hippocampus following a single systemic kainic acid (KA) administration. In addition, we showed that blocking of all PG productions ameliorated hippocampal delayed neuronal death at 30 days after KA administration...
February 7, 2017: Journal of Lipid Research
https://www.readbyqxmd.com/read/28170441/cerebrospinal-fluid-from-patients-with-amyotrophic-lateral-sclerosis-inhibits-sonic-hedgehog-function
#18
Anna Drannik, Joan Martin, Randy Peterson, Xiaoxing Ma, Fan Jiang, John Turnbull
Sonic hedgehog (Shh) is a morphogen essential to the developing nervous system that continues to play an important role in adult life by contributing to cell proliferation and differentiation, maintaining blood-brain barrier integrity, and being cytoprotective against oxidative and excitotoxic stress, all features of importance in amyotrophic lateral sclerosis (ALS). ALS is a fatal disease characterized by selective loss of motor neurons due to poorly understood mechanisms. Evidence indicates that Shh might play an important role in ALS, and that Shh signaling might be also adversely affected in ALS...
2017: PloS One
https://www.readbyqxmd.com/read/28167117/protection-against-alcohol-induced-neuronal-and-cognitive-damage-by-the-ppar%C3%AE-receptor-agonist-pioglitazone
#19
Andrea Cippitelli, Esi Domi, Massimo Ubaldi, James C Douglas, Hong Wu Li, Gregory Demopulos, George Gaitanaris, Marisa Roberto, Paul D Drew, Cynthia J M Kane, Roberto Ciccocioppo
Binge alcohol drinking has emerged as a typical phenomenon in young people. This pattern of drinking, repeatedly leading to extremely high blood and brain alcohol levels and intoxication is associated with severe risks of neurodegeneration and cognitive damage. Mechanisms involved in excitotoxicity and neuroinflammation are pivotal elements in alcohol-induced neurotoxicity. Evidence has demonstrated that PPARγ receptor activation shows anti-inflammatory and neuroprotective properties. Here we examine whether treatment with the PPARγ agonist pioglitazone is beneficial in counteracting neurodegeneration, neuroinflammation and cognitive damage produced by binge alcohol intoxication...
February 3, 2017: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/28161868/protective-effect-of-resveratrol-on-the-brain-in-a-rat-model-of-epilepsy
#20
Zhen Li, Zhuyan You, Min Li, Liang Pang, Juan Cheng, Liecheng Wang
Accumulating evidence has suggested resveratrol as a promising drug candidate for the treatment of epilepsy. To validate this, we tested the protective effect of resveratrol on a kainic acid (KA)-induced epilepsy model in rats and investigated the underlying mechanism. We found that acute resveratrol application partially inhibited evoked epileptiform discharges in the hippocampal CA1 region. During acute, silent and chronic phases of epilepsy, the expression of hippocampal kainate glutamate receptor (GluK2) and the GABAA receptor alpha1 subunit (GABAAR-alpha1) was up-regulated and down-regulated, respectively...
February 4, 2017: Neuroscience Bulletin
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