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题名: Calcium-activated NO Production Plays a Role in Neuronal Death Induced by β-bungarotoxin in Primary Cultures of Cerebellar Granular Neurons
作者: Tseng, Wen-Pei;Shoei-Yn Lin-Shiau
贡献者: 運動健康所
关键词: β-bungarotoxin;NMDAR activation;Calcium overloading;Nitric oxide;Neurotoxicity
日期: 2003-05
上传时间: 2014-01-15T04:02:40Z
出版者: Springer
摘要: The aim of this study was to elucidate the
mechanism underlying the neurotoxic effect of β-bungarotoxin
(β-BuTX) on cultured cerebellar granular neurons
(CGN). β-BuTX had a potent time- and concentrationdependent
neurotoxic effect on mature CGN. β-BuTX appeared
to destroy initially the neurites and then caused
neuronal death by both apoptotic and necrotic processes.
Inspection using Nomarski optics showed that these neurons
displayed morphological features of necrotic cells,
including cell swelling, loss of membrane integrity and
eventual dissolution of the cell. Staining with the fluorescent
dye Hoechst 33258 showed that β-BuTX-treated neuron
bodies stained more densely with smaller apoptotic
bodies. Using microspectrofluorimetry and fura-2 to measure
cytosolic [Ca2+] ([Ca2+]i), β-BuTX markedly increased
[Ca2+]i. BAPTA-AM, EGTA, MK 801 and diltiazem not
only attenuated the β-BuTX-mediated rise in [Ca2+]i but
also attenuated β-BuTX-mediated neurotoxicity. In addition,
these Ca2+ inhibitors prevented the β-BuTX-induced
generation of reactive nitrogen species. The NO synthase
inhibitor NG-methyl-L-arginine) also exhibited neuroprotection.
This is the first report showing that β-BuTX-induced
CGN death is mediated, at least in part, by excessive
generation of NO triggered by [Ca2+]i overloading.
Activation of NMDA receptors and L-type calcium channels
is apparently involved in the increase in [Ca2+]i induced
by this neurotoxin. This potent neurotoxin will be a
useful tool for studying neurotoxic processes and using
this model system will allow us to find neuroprotective
關聯: Naunyn-Schmiedeberg’s Arch Pharmacol, 367(5): 451-461
显示于类别:[運動健康研究所] 期刊論文


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