Excitotoxicity
Mostrando 1-12 de 62 artigos, teses e dissertações.
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1. Neuroprotective properties of RT10, a fraction isolated from Parawixia bistriata spider venom, against excitotoxicity injury in neuron-glia cultures
Abstract Background: L-Glutamate (L-Glu), the major excitatory neurotransmitter in the mammalian Central Nervous System (CNS), is essential to cognitive functions. However, when L-Glu is accumulated in large concentrations at the synaptic cleft, it can induce excitotoxicity that results in secondary damage implicated in many neurological disorders. Current
J. Venom. Anim. Toxins incl. Trop. Dis. Publicado em: 16/05/2019
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2. Amburana cearensis seed extracts protect PC-12 cells against toxicity induced by glutamate
ABSTRACT Amburana cearensis (Allemão) A.C. Sm., Fabaceae, has been widely studied for its medicinal activities. Many neurodegenerative disorders are caused by oxidative stress, mitochondrial dysfunction, excitotoxicity induced by glutamate and ultimately cell death. This study describes the chemical profile of the ethanolic, hexane, dichloromethane, and eth
Rev. bras. farmacogn.. Publicado em: 2017-04
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3. Neuroprotection of Persea major extract against oxygen and glucose deprivation in hippocampal slices involves increased glutamate uptake and modulation of A1 and A2A adenosine receptors
Ischemic stroke is characterised by a lack of oxygen and glucose in the brain, leading to excessive glutamate release and neuronal cell death. Adenosine is produced in response to ATP depletion and acts as an endogenous neuromodulator that reduces excitotoxicity. Persea major (Meins.) L.E. Kopp (Lauraceae) is a medical plant that is indigenous to South Brazi
Rev. bras. farmacogn.. Publicado em: 2013-10
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4. A metanandamida, um agonista canabinóide, protege a linhagem de neuroblastoma neuro2A da morte celular induzida por peróxido de hidrogênio. / The methanandamide, a cannabinoid agonist, protect the lineage of neuro 2A cell death induced by hydrogen peroxide.
Neurodegenerative diseases are progressive disorder affecting specific neuronal populations in the central nervous system, leading to neuronal death. Several factors contribute to the development of neurodegenerative diseases, including increased free radical formation and / or oxidative stress. The cannabinoid system has been suggested as an important syste
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 02/07/2012
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5. Envolvimento de Rac1 na excitotoxicidade induzida por NMDA na retina de ratos. / Involvement of Rac1 in NMDA-induced excitotoxicity in the rat retina.
A ativação excessiva dos receptores NMDA tem sido descrita no disparo da morte neuronal que ocorre em doenças, como o glaucoma. É possível que a combinação de subunidades (NR2A-D) possa ativar vias de sinalização intracelulares que resultam na morte ou sobrevivência. Nosso objetivo foi investigar o envolvimento de subunidades NR2 e Rac1, membro da
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 19/09/2011
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6. Efeito da inibição da enzima JAK2 sobre a morte neuronal, astrogliose e neurogênese no estriado de camundongos adultos após injeção unilateral de ácido quinolínico / Effect of JAK2 enzyme inhibition on neuronal death, astrogliosis and neurogenesis in the striatum of adult mice after unilateral injection of quinolinic acid
A injeção de ácido quinolínico (AQ), um agonista glutamatérgico do receptor N-metil-D-aspartato, no estriado de roedores induz morte seletiva de neurônios espinhosos médios, gliose reativa e neurogênese na zona subventricular, acompanhada da migração dos neurônios recém-gerados para o estriado lesado. Tais achados são também descritos na doenç
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 22/06/2011
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7. Participação das vias de estresse oxidativo na neuroproteção mediada pelo treinamento físico em fatias cerebrais submetidas à privação de oxigênio e glicose
Ischemia leads to a variety of pathological events, including excitotoxicity, inflammation, delayed neuronal dysfunction and cell death through hyperactivation of glutamate receptors and production of free radicals, such as nitric oxide (NO). The mechanism by which cerebral excess formation of NO, which mediates neuronal death involving energy depletion, lip
Publicado em: 2011
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8. EFEITO NEUROPROTETOR DA CREATINA E AVALIAÇÃO DOS PARÂMETROS CINÉTICOS DA CAPTAÇÃO DE GLUTAMATO INDUZIDOS PELO ÁCIDO GLUTÁRICO NO ESTRIADO DE RATOS / NEUROPROTECTIVE EFFECT OF CREATINE AND EVALUATION OF KINETIC PARAMETERS OF GLUTAMATE UPTAKE INDUCED BY GLUTARIC ACID FROM STRIATUM THE RATS
A acidemia glutárica tipo I (GA-I) é um erro inato do metabolismo (EIM) caracterizada bioquimicamente pelo acúmulo principal de ácido glutárico (GA) e ácido 3-hidroxiglutárico (3-OH-GA), e patologicamente por uma característica degeneração estriatal. Devido à escassez de medidas terapêuticas efetivas para essa acidemia, vários estudos têm inves
Publicado em: 2008
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9. Possible etiologies for tropical spastic paraparesis and human T lymphotropic virus I-associated myelopathy
The epidemiology of tropical spastic paraparesis/human T lymphotropic virus I (HTLV-I)-associated myelopathy (TSP/HAM) is frequently inconsistent and suggests environmental factors in the etiology of these syndromes. The neuropathology corresponds to a toxometabolic or autoimmune process and possibly not to a viral disease. Some logical hypotheses about the
Brazilian Journal of Medical and Biological Research. Publicado em: 2004-01
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10. Role of metabotropic glutamate receptors in oligodendrocyte excitotoxicity and oxidative stress
Developing oligodendrocytes (OLs) are highly vulnerable to excitotoxicity and oxidative stress, both of which are important in the pathogenesis of many brain disorders. OL excitotoxicity is mediated by ionotropic glutamate receptors (iGluRs) of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/kainate type on these cells. Here we report that metabotr
National Academy of Sciences.
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11. Presenilin-1 regulates the neuronal threshold to excitotoxicity both physiologically and pathologically
A direct pathophysiological role of Familial Alzheimer's Disease (FAD)-associated Presenilin 1 (PS1) mutations in neuronal vulnerability remains a controversial matter. We evaluated the relationship between PS1 and excitotoxicity in four different experimental models of neurotoxicity by using primary neurons from (i) transgenic (tg) mice overexpressing
The National Academy of Sciences.
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12. Tyrosine phosphatase SHP-2 is a mediator of activity-dependent neuronal excitotoxicity
Calcium influx can promote neuronal differentiation and survival, at least in part by activating Ras and its downstream targets, including the Erk pathway. However, excessive calcium influx can initiate molecular signals leading to neuronal death during excitotoxicity or in neurodegenerative diseases. Here we describe a new signaling pathway associated with
Nature Publishing Group.