Glutamate release by an Na<sup>+</sup> load and oxidative stress in nerve terminals: relevance to ischemia/reperfusion

Tretter, László; Ádám-Vizi, Vera

doi:10.1046/j.1471-4159.2002.01191.x

Cited by 24 publications

(12 citation statements)

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“…17,18 Ion channels such as glutamate N-methyl-d-aspartate (NMDA) or the voltagegated Ca 2+ channel or Na + channel are considered to be involved in these processes. 32,33,43 An ionotropic glutamatergic receptor antagonist, such as MK801, has been shown to have a neuroprotective effect against retinal ischemic insult.…”

Section: Discussionmentioning

confidence: 99%

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Neuroprotective Effect of the Novel Na+/Ca2+ Channel Blocker NS-7 on Rat Retinal Ganglion Cells

et al. 2005

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Section: Discussionmentioning

confidence: 99%

“…Ischemia-reperfusion injury to the retina is the commonly used in vivo model for investigating the RGC damage mechanism [14][15][16][17][18][19] and drug effects on RGC damage. The present study was designed to investigate whether NS-7 has neuroprotective effects on rat RGCs , using the ischemia-reperfusion injury model of rat retinal ganglion cells.…”

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confidence: 99%

Neuroprotective Effect of the Novel Na+/Ca2+ Channel Blocker NS-7 on Rat Retinal Ganglion Cells

et al. 2005

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“…Por outro lado, outros estudos mostram que receptores NMDA possuem um sítio modulatório redox-sensível que, quando oxidado, diminui a atividade do receptor 53,54 . Alguns autores sugerem que a influência das ROS sobre receptores NMDA pode ter papel importante em determinadas situações patológicas como a isquemia/reperfusão onde há um aumento considerável na produção de tais espécies com conseqüente excitotoxicidade mediada pelo glutamato 53,54,64,72,73,74 . Contudo, o efeito líquido das ROS sobre a atividade de receptores NMDA em condições fisiológicas parece depender de fatores ainda não bem esclarecidos.…”

Section: -Modificações Oxidativasunclassified

Espécies Reativas De Oxigênio No Controle Neurovegetativo Da Pressão Arterial

Cardoso

Colombari

Menani

et al. 2006

Medicina (Ribeirão Preto)

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RESUMO: Existem evidências de que a atividade neuronal pode ser modulada pelo estado redox (balanço entre espécies químicas oxidantes e redutoras) das células, influenciando, assim, as diferentes funções biológicas que são controladas pelo sistema nervoso. Essa modulação pode ocorrer por meio de diferentes mecanismos e um deles é a modulação da transmissão sináptica no sistema nervoso central (SNC). As descargas autonômicas que são controladas por mecanismos localizados em diferentes áreas do SNC são fundamentais para o controle da pressão arterial. Um importante neurotransmissor que participa dos mecanismos centrais de controle cardiovascular é o glutamato e a transmissão glutamatérgica pode ser extensamente afetada por espécies reativas de oxigênio, oxidantes que parecem ter um importante papel em processos fisiológicos e patológicos. No presente artigo são apresentados os principais achados experimentais que suportam a hipótese de que as espécies reativas de oxigênio podem modular as funções cardiovasculares por produzir alterações nos mecanismos centrais de controle dos sistemas simpático e parassimpático. Logo, desequilíbrios na sinalização mediada por espécies reativas de oxigênios podem contribuir para o desenvolvimento de doenças cardiovasculares como a hipertensão.

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“…Compounds that possess antioxidative activity might offer benefits in preventing or retarding some brain disorders since free radical-induced oxidative damage to the brain has been regarded as an important cause of neuronal death in a variety of neurodegenerative disorders as well as in ischemia and in the aging process [8,9] . Furthermore, this oxidative injury is reported to be associated with an excess release of glutamate [10,11] .…”

Section: Introductionmentioning

confidence: 99%

HTDP-2, a New Synthetic Compound, Inhibits Glutamate Release through Reduction of Voltage-Dependent Ca<sup>2+</sup> Influx in Rat Cerebral Cortex Nerve Terminals

Lin

Huang

et al. 2011

Pharmacology

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Aim: The present study was aimed at investigating the effect of trans-6-(4-chlorobutyl)-5-hydroxy-4-(phenylthio)-1-tosyl-5,6-dihydropyridine-2(1H)-one (HTDP-2), a novel synthetic compound, on the release of endogenous glutamate in rat cerebrocortical nerve terminals (synaptosomes) and exploring the possible mechanism. Methods: The release of glutamate was evoked by the K⁺ channel blocker 4-aminopyridine (4-AP) and measured by an on-line enzyme-coupled fluorimetric assay. We also used a membrane potential-sensitive dye to assay nerve terminal excitability and depolarization, and a Ca²⁺ indicator, Fura-2-acetoxymethyl ester, to monitor cytosolic Ca²⁺ concentrations ([Ca²⁺]_c). Results: HTDP-2 inhibited the release of glutamate evoked by 4-AP in a concentration-dependent manner. Inhibition of glutamate release by HTDP-2 was prevented by the chelating intraterminal Ca²⁺ ions, and by the vesicular transporter inhibitor bafilomycin A1, but was insensitive to the glutamate transporter inhibitor DL-threo-β-benzyloxyaspartate. HTDP-2 did not alter the resting synaptosomal membrane potential or 4-AP-mediated depolarization whereas it decreased the 4-AP-induced increase in [Ca²⁺]_c. Furthermore, the inhibitory effect of HTDP-2 on the evoked glutamate release was abolished by the N-, and P/Q-type Ca²⁺ channel blocker ω-conotoxin MVIIC, but not by the ryanodine receptor blocker dantrolene, or the mitochondrial Na⁺/Ca²⁺ exchanger blocker CGP37157. Conclusion: Based on these results, we suggest that, in rat cerebrocortical nerve terminals, HTDP-2 decreases voltage-dependent Ca²⁺ channel activity and, in so doing, inhibits the evoked glutamate release.

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Glutamate release by an Na⁺ load and oxidative stress in nerve terminals: relevance to ischemia/reperfusion

Cited by 24 publications

References 50 publications

Neuroprotective Effect of the Novel Na+/Ca2+ Channel Blocker NS-7 on Rat Retinal Ganglion Cells

Neuroprotective Effect of the Novel Na+/Ca2+ Channel Blocker NS-7 on Rat Retinal Ganglion Cells

Espécies Reativas De Oxigênio No Controle Neurovegetativo Da Pressão Arterial

HTDP-2, a New Synthetic Compound, Inhibits Glutamate Release through Reduction of Voltage-Dependent Ca<sup>2+</sup> Influx in Rat Cerebral Cortex Nerve Terminals

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Glutamate release by an Na+ load and oxidative stress in nerve terminals: relevance to ischemia/reperfusion

Cited by 24 publications

References 50 publications

Neuroprotective Effect of the Novel Na+/Ca2+ Channel Blocker NS-7 on Rat Retinal Ganglion Cells

Neuroprotective Effect of the Novel Na+/Ca2+ Channel Blocker NS-7 on Rat Retinal Ganglion Cells

Espécies Reativas De Oxigênio No Controle Neurovegetativo Da Pressão Arterial

HTDP-2, a New Synthetic Compound, Inhibits Glutamate Release through Reduction of Voltage-Dependent Ca<sup>2+</sup> Influx in Rat Cerebral Cortex Nerve Terminals

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Glutamate release by an Na⁺ load and oxidative stress in nerve terminals: relevance to ischemia/reperfusion