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Excitotoxicity

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https://www.readbyqxmd.com/read/28543944/anterior-cingulate-cortex-supports-effort-allocation-toward-a-qualitatively-preferred-option
#1
Evan E Hart, Julian O Gerson, Yael Zoken, Marisella Garcia, Alicia Izquierdo
The anterior cingulate cortex (ACC) is known to be involved in effortful choice, yet its role in cost-benefit evaluation of qualitatively different rewards (more/less preferred), beyond magnitude differences (larger/smaller), is poorly understood. Selecting between qualitatively different options is a decision type commonly faced by humans. Here we assessed the role of ACC on a task that has primarily been used to probe striatal function in motivation. Rats were trained to stable performance on a progressive ratio schedule for sucrose pellets and were then given sham surgeries (control) or excitotoxic NMDA-lesions of ACC...
May 20, 2017: European Journal of Neuroscience
https://www.readbyqxmd.com/read/28540665/different-molecular-mechanisms-mediate-direct-or-glia-dependent-prion-protein-fragment-90-231-neurotoxic-effects-in-cerebellar-granule-neurons
#2
Stefano Thellung, Elena Gatta, Francesca Pellistri, Valentina Villa, Alessandro Corsaro, Mario Nizzari, Mauro Robello, Tullio Florio
Glia over-stimulation associates with amyloid deposition contributing to the progression of central nervous system neurodegenerative disorders. Here we analyze the molecular mechanisms mediating microglia-dependent neurotoxicity induced by prion protein (PrP)90-231, an amyloidogenic polypeptide corresponding to the protease-resistant portion of the pathological prion protein scrapie (PrP(Sc)). PrP90-231 neurotoxicity is enhanced by the presence of microglia within neuronal culture, and associated to a rapid neuronal [Ca(++)] i increase...
May 25, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28540131/parkinson-s-disease-microglial-macrophage-induced-immunoexcitotoxicity-as-a-central-mechanism-of-neurodegeneration
#3
REVIEW
Russell L Blaylock
Parkinson's disease is one of the several neurodegenerative disorders that affects aging individuals, with approximately 1% of those over the age of 60 years developing the disorder in their lifetime. The disease has the characteristics of a progressive disorder in most people, with a common pattern of pathological change occurring in the nervous system that extends beyond the classical striatal degeneration of dopaminergic neurons. Earlier studies concluded that the disease was a disorder of alpha-synuclein, with the formation of aggregates of abnormal alpha-synuclein being characteristic...
2017: Surgical Neurology International
https://www.readbyqxmd.com/read/28539424/ca-2-permeable-ampars-mediate-glutamatergic-transmission-and-excitotoxic-damage-at-the-hair-cell-ribbon-synapse
#4
Joy Y Sebe, Soyoun Cho, Lavinia Sheets, Mark A Rutherford, Henrique von Gersdorff, David W Raible
We report functional and structural evidence for GluA2-lacking Ca(2+)-permeable AMPARs (CP-AMPARs) at the mature hair cell ribbon synapse. By utilizing the methodological advantages of three species (of either sex), we demonstrate that CP-AMPARs are present at the hair cell synapse in an evolutionarily conserved manner. Via a combination of in vivo electrophysiological and Ca(2+) imaging approaches in the larval zebrafish, we show that hair cell stimulation leads to robust Ca(2+) influx into afferent terminals...
May 24, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28536976/memory-and-learning-dysfunction-following-copper-toxicity-biochemical-and-immunohistochemical-basis
#5
Jayantee Kalita, Vijay Kumar, Usha K Misra, Himangsu K Bora
The prototype disease of Cu toxicity in human is Wilson disease, and cognitive impairment is the presenting symptom of it. There is no study correlating Cu-induced excitotoxicity, apoptosis, and astrocytic reaction with memory dysfunction. We report excitotoxicity, apoptosis, and astrocytic reaction of the hippocampus and frontal cortex with memory dysfunction in rat model of Cu toxicity. Thirty-six rats were divided into group I (control) and group II (100 mg/kgBwt/day CuSO4 orally). Y-maze was performed for memory and learning at 0, 30, 60, and 90 days...
May 23, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28535416/the-role-of-timing-in-the-treatment-of-spinal-cord-injury
#6
REVIEW
Amene Saghazadeh, Nima Rezaei
Regeneration failure after primary spinal cord injury (SCI) leads to diverse clinical complications in a severity- and level of SCI-dependent manner. The cost of treating both of them (initial regeneration failure and following complications) would be prohibitive, particularly in less developed nations. The well-recognized circumstances arose from primary SCI include excitotoxicity and inflammation. SCI increases concentrations of extracellular amino acids (EAAs) in the severity-dependent manner and the maximum level of EAAs at the injury site will be reduced by distance from the injury site...
May 20, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28533113/a-novel-serine-racemase-inhibitor-suppresses-neuronal-over-activation-in-vivo
#7
Hisashi Mori, Ryogo Wada, Satoyuki Takahara, Yoshikazu Horino, Hironori Izumi, Tetsuya Ishimoto, Tomoyuki Yoshida, Mineyuki Mizuguchi, Takayuki Obita, Hiroaki Gouda, Shuichi Hirono, Naoki Toyooka
Serine racemase (SRR) is an enzyme that produces d-serine from l-serine. d-Serine acts as an endogenous coagonist of NMDA-type glutamate receptors (NMDARs), which regulate many physiological functions. Over-activation of NMDARs induces excitotoxicity, which is observed in many neurodegenerative disorders and epilepsy states. In our previous works on the generation of SRR gene knockout (Srr-KO) mice and its protective effects against NMDA- and Aβ peptide-induced neurodegeneration, we hypothesized that the regulation of NMDARs' over-activation by inhibition of SRR activity is one such therapeutic strategy to combat these disease states...
May 11, 2017: Bioorganic & Medicinal Chemistry
https://www.readbyqxmd.com/read/28532421/glutamate-excitotoxicity-induced-by-orally-administered-propionic-acid-a-short-chain-fatty-acid-can-be-ameliorated-by-bee-pollen
#8
Afaf El-Ansary, Huda S Al-Salem, Alqahtani Asma, Abeer Al-Dbass
BACKGROUND: Rodent models may guide investigations towards identifying either environmental neuro-toxicants or drugs with neuro-therapeutic effects. This work aims to study the therapeutic effects of bee pollen on brain glutamate excitotoxicity and the impaired glutamine-glutamate- gamma amino butyric acid (GABA) circuit induced by propionic acid (PPA), a short chain fatty acid, in rat pups. METHODS: Twenty-four young male Western Albino rats 3-4 weeks of age, and 45-60 g body weight were enrolled in the present study...
May 22, 2017: Lipids in Health and Disease
https://www.readbyqxmd.com/read/28531131/the-role-of-interleukin-18-oxidative-stress-and-metabolic-syndrome-in-alzheimer-s-disease
#9
REVIEW
Johanna O Ojala, Elina M Sutinen
The role of interleukins (ILs) and oxidative stress (OS) in precipitating neurodegenerative diseases including sporadic Alzheimer's disease (AD), requires further clarification. In addition to neuropathological hallmarks-extracellular neuritic amyloid-β (Aβ) plaques, neurofibrillary tangles (NFT) containing hyperphosphorylated tau and neuronal loss-chronic inflammation, as well as oxidative and excitotoxic damage, are present in the AD brain. The pathological sequelae and the interaction of these events during the course of AD need further investigation...
May 21, 2017: Journal of Clinical Medicine
https://www.readbyqxmd.com/read/28527955/neuroprotective-effect-of-the-alpha-7-nicotinic-receptor-agonist-pha-543613-in-an-in-vivo-excitotoxic-adult-rat-model
#10
Laura Foucault-Fruchard, Aurélie Doméné, Guylène Page, Marguerite Windsor, Patrick Emond, Nuno Rodrigues, Frédéric Dollé, Annelaure Damont, Frédéric Buron, Sylvain Routier, Sylvie Chalon, Daniel Antier
Neuroinflammation is a key component of the pathophysiology of neurodegenerative diseases. The link between nicotine intake and positive outcome has been established, suggesting a role played by nicotinic receptors (nAChRs), especially α7nAChRs. The objective of this study was to evaluate the potential dose effects of PHA 543613 on neuron survival and striatal microglial activation in a rat model of brain excitotoxicity. A preliminary study was performed in vitro to confirm PHA 543613 agonist properties on α7nAChRs...
May 17, 2017: Neuroscience
https://www.readbyqxmd.com/read/28526579/differential-involvement-of-vesicular-and-glial-glutamate-transporters-around-spinal-%C3%AE-motoneurons-in-the-pathogenesis-of-sod1-g93a-mouse-model-of-amyotrophic-lateral-sclerosis
#11
Tomohiro Ohgomori, Ryo Yamasaki, Hideyuki Takeuchi, Kenji Kadomatsu, Jun-Ichi Kira, Shozo Jinno
From a view point of the glutamate excitotoxicity theory, several studies have suggested that abnormal glutamate homeostasis via dysfunction of glial glutamate transporter-1 (GLT-1) may underlie neurodegeneration in amyotrophic lateral sclerosis (ALS). However, the detailed role of GLT-1 in the pathogenies of ALS remains controversial. To assess this issue, here we elucidated structural alterations associated with dysregulation of glutamate homeostasis using SOD1(G93A) mice, a genetic model of familial ALS...
May 16, 2017: Neuroscience
https://www.readbyqxmd.com/read/28526038/phosphorylation-of-tau-at-y18-but-not-tau-fyn-binding-is-required-for-tau-to-modulate-nmda-receptor-dependent-excitotoxicity-in-primary-neuronal-culture
#12
Takashi Miyamoto, Liana Stein, Reuben Thomas, Biljana Djukic, Praveen Taneja, Joseph Knox, Keith Vossel, Lennart Mucke
BACKGROUND: Hyperexcitability of neuronal networks can lead to excessive release of the excitatory neurotransmitter glutamate, which in turn can cause neuronal damage by overactivating NMDA-type glutamate receptors and related signaling pathways. This process (excitotoxicity) has been implicated in the pathogenesis of many neurological conditions, ranging from childhood epilepsies to stroke and neurodegenerative disorders such as Alzheimer's disease (AD). Reducing neuronal levels of the microtubule-associated protein tau counteracts network hyperexcitability of diverse causes, but whether this strategy can also diminish downstream excitotoxicity is less clear...
May 19, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28523591/assessment-of-the-neuroprotective-effects-of-arginine-rich-protamine-peptides-poly-arginine-peptides-r12-cyclic-r22-and-arginine-tryptophan-containing-peptides-following-in-vitro-excitotoxicity-and-or-permanent-middle-cerebral-artery-occlusion-in-rats
#13
Bruno P Meloni, Diego Milani, Jane L Cross, Vince W Clark, Adam B Edwards, Ryan S Anderton, David J Blacker, Neville W Knuckey
We have demonstrated that arginine-rich and poly-arginine peptides possess potent neuroprotective properties with arginine content and peptide positive charge being particularly critical for neuroprotective efficacy. In addition, the presence of other amino acids within arginine-rich peptides, as well as chemical modifications, peptide length and cell-penetrating properties also influence the level of neuroprotection. Against this background, we have examined the neuroprotective efficacy of arginine-rich protamine peptides, a cyclic (R12-c) poly-arginine peptide and a R22 poly-arginine peptide, as well as arginine peptides containing tryptophan or other amino acids (phenylalanine, tyrosine, glycine or leucine) in in vitro glutamic acid excitotoxicity and in vivo rat permanent middle cerebral artery occlusion models of stroke...
May 18, 2017: Neuromolecular Medicine
https://www.readbyqxmd.com/read/28523551/epigenetic-mechanisms-of-gene-regulation-in-amyotrophic-lateral-sclerosis
#14
Alba Jimenez-Pacheco, Jaime M Franco, Soledad Lopez, Juan Miguel Gomez-Zumaquero, Maria Magdalena Leal-Lasarte, Diana E Caballero-Hernandez, Marta Cejudo-Guillén, David Pozo
Despite being clinically described 150 years ago, the mechanisms underlying amyotrophic lateral sclerosis (ALS) pathogenesis have not yet been fully understood. Studies in both animal models of ALS and human patients reveal a plethora of alterations such as increased glutamate-mediated excitotoxicity, redox stress, increased apoptosis, defective axonal transport, protein-misfolding events, mitochondrial impairment and sustained unregulated immune responses. Regardless of being sporadic or familiar ALS, the final outcome at the cellular level is the death of upper and lower motor neurons, and once diagnosed, ALS is typically lethal within the next 5 years...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28522414/therapeutic-potential-of-agmatine-for-cns-disorders
#15
REVIEW
Vivian B Neis, Priscila B Rosa, Gislaine Olescowicz, Ana Lúcia S Rodrigues
Agmatine is a neuromodulator that regulates multiple neurotransmitters and signaling pathways. Several studies have focused on elucidating the mechanisms underlying the neuroprotective effects of this molecule, which seems to be mediated by a reduction in oxidative damage, neuroinflammation, and proapoptotic signaling. Since these events are implicated in acute and chronic excitotoxicity-related disorders (ischemia, epilepsy, traumatic brain injury, spinal cord injury, neurodegenerative, and psychiatric disorders) as well as in nociception, agmatine has been proposed as a therapeutic strategy for the treatment of central nervous system (CNS) disorders...
May 15, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28512742/differing-intrinsic-biological-properties-between-forebrain-and-spinal-oligodendroglial-lineage-cells
#16
Makoto Horiuchi, Yoko Suzuki-Horiuchi, Tasuku Akiyama, Aki Itoh, David Pleasure, Earl Carstens, Takayuki Itoh
Differentiation of oligodendroglial progenitor cells (OPCs) into myelinating oligodendrocytes is known to be regulated by the microenvironment where they differentiate. However, current research has not verified whether or not oligodendroglial lineage cells (OLCs) derived from different anatomical regions of the central nervous system (CNS) respond to microenvironmental cues in the same manner. Here, we isolated pure OPCs from rat neonatal forebrain (FB) and spinal cord (SC) and compared their phenotypes in the same in vitro conditions...
May 17, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28511980/reward-loss-and-the-basolateral-amygdala-a-function-in-reward-comparisons
#17
Katsuyoshi Kawasaki, Iván Annicchiarico, Amanda C Glueck, Ignacio Morón, Mauricio R Papini
The neural circuitry underlying behavior in reward loss situations is poorly understood. We considered two such situations: reward devaluation (from large to small rewards) and reward omission (from large rewards to no rewards). There is evidence that the central nucleus of the amygdala (CeA) plays a role in the negative emotion accompanying reward loss. However, little is known about the function of the basolateral nucleus (BLA) in reward loss. Two hypotheses of BLA function in reward loss, negative emotion and reward comparisons, were tested in an experiment involving pretraining excitotoxic BLA lesions followed by training in four tasks: consummatory successive negative contrast (cSNC), autoshaping (AS) acquisition and extinction, anticipatory negative contrast (ANC), and open field testing (OF)...
May 13, 2017: Behavioural Brain Research
https://www.readbyqxmd.com/read/28511953/small-conductance-ca-2-activated-k-channels-in-the-plasma-membrane-mitochondria-and-the-er-pharmacology-and-implications-in-neuronal-diseases
#18
REVIEW
Birgit Honrath, Inge Krabbendam, Carsten Culmsee, Amalia Dolga
Ca(2+)-activated K(+) (KCa) channels regulate after-hyperpolarization in many types of neurons in the central and peripheral nervous system. Small conductance Ca(2+)-activated K(+) (KCa2/SK) channels, a subfamily of KCa channels, are widely expressed in the central and peripheral nervous system, and in the cardiovascular system. Voltage-independent SK channels are activated by alterations in intracellular Ca(2+) ([Ca(2+)]i) which facilitates the opening of these channels through binding of Ca(2+) to calmodulin that is constitutively bound to the SK2 C-terminus...
May 13, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28511127/neurophysiology-of-synaptic-functioning-in-multiple-sclerosis
#19
REVIEW
Mario Stampanoni Bassi, Francesco Mori, Fabio Buttari, Girolama A Marfia, Andrea Sancesario, Diego Centonze, Ennio Iezzi
Multiple sclerosis (MS) is an inflammatory immune-mediate disorder of the central nervous system (CNS), primarily affecting the myelin sheath and followed by neurodegeneration. Synaptic alterations are emerging as critical determinants of early neurodegeneration in MS. Inflammation-induced alterations of synaptic transmission and plasticity have been investigated in vitro and also in human MS using transcranial magnetic stimulation (TMS) techniques. Specific inflammatory cytokines alter glutamatergic and GABAergic transmission, resulting in synaptic hyperexcitability...
April 24, 2017: Clinical Neurophysiology: Official Journal of the International Federation of Clinical Neurophysiology
https://www.readbyqxmd.com/read/28508312/trpc-channels-and-programmed-cell-death
#20
Jian Zhou, Yichang Jia
Neurotrophins, including nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), bind to their high-affinity receptors to promote neuronal survival during brain development. One of the key downstream pathways is the phospholipase C (PLC) pathway, which not only plays a central role in calcium release from internal store but also in activation of TRPC channels coupled with neurotrophin receptors. TRPC channels are required for the neurotrophin-mediated neuronal protective effects. In addition, activation of TRPC channels is able to protect neurons in the absence of neurotrophin...
2017: Advances in Experimental Medicine and Biology
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