乙型雨傘節蛇毒毒素引發小腦顆粒神經細胞毒性之訊息傳遞途徑研究 ; Studies on Signal Transduction Pathway of b-Bungarotoxin-induced Neurotoxicity in the Cultured Cerebellar Granule Neurons

التفاصيل البيبلوغرافية
العنوان: 乙型雨傘節蛇毒毒素引發小腦顆粒神經細胞毒性之訊息傳遞途徑研究 ; Studies on Signal Transduction Pathway of b-Bungarotoxin-induced Neurotoxicity in the Cultured Cerebellar Granule Neurons
المؤلفون: 曾文培
المساهمون: 運動健康所
بيانات النشر: 國立台灣大學
سنة النشر: 2002
المجموعة: National Changhua University of Education Institutional Repository
مصطلحات موضوعية: b-Bungarotoxin, Cerebellar Granule Neurons, Intracellular calcium, Reactive oxygen species, Nitric Oxide, Apoptosis, Neurotoxicity, Siganl transduction, 乙型雨傘節蛇毒毒素, 小腦顆粒神經細胞, 細胞內鈣離子濃度, 活性氧化物質, 一氧化氮, 細胞凋亡, 神經毒性, 訊息傳遞
الوقت: 50
الوصف: The aim of this study is to elucidate the mechanism of neurotoxic effect of β-bungarotoxin on the cultured cerebellar granule neurons. β-BuTX exerted a potent neurotoxic effect upon mature granule neurons. Quantitative analysis of neurotoxicity revealed the time- and concentration-dependency. It is noted that β-BuTX appeared to initially destroy the neurite and then caused the neuronal death mediated by both apoptosis and necrosis processes. Nomarski optics showed that these neurons displayed morphological features of necrotic cells, including cell swelling, destruction of membrane integrity and eventual dissolution of the cell. Staining with the fluorescent dye Hoechst 33258 showed that β-BuTX-treated neuron body had a higher densed staining with smaller apoptotic bodies. Using microspectrofluorimetry and fura-2 to measure [Ca2+]i, we found that β-BuTX markedly increased [Ca2+]i. Furthermore, BAPTA-AM, EGTA, MK 801 and diltiazem not only inhibit the elevated [Ca2+]i but also attenuate the neurotoxicity of β-BuTX. Moreover, these Ca2+ inhibitors prevent the β-BuTX-induced reactive nitrogenous species production and NO synthase inhibitor (NG-methyl-L-arginine) exhibits the neuroprotection. Therefore, we conclude for the first report that β-BuTX-induced cerebellar granule neuron death is mediated by, at least in part, excessive generation of nitric oxide triggered by [Ca2+]i overloading. The activation of NMDA receptor and L-type calcium channel apparently involved in increasing [Ca2+]i induced by this neurotoxin. We suggest that this potent neurotoxin is a useful tool for us to study the neurotoxic process and thus we will be able to find the neuroprotective agent by using this model system. Neuronal death signaling through activating NMDA receptor and L-type calcium channel induced by β-bungarotoxin The aim of this study is to elucidate the mechanism of neurotoxic effect of β-bungarotoxin (β-BuTX, a snake presynaptic neurotoxin isolated from the venom of Bungarus multicintus) on the cultured cerebellar granule ...
نوع الوثيقة: other/unknown material
وصف الملف: application/pdf; 165882 bytes
اللغة: English
العلاقة: 博士; 國立台灣大學藥理學研究所; http://ir.ncue.edu.tw/ir/handle/987654321/17861Test
الإتاحة: http://ir.ncue.edu.tw/ir/handle/987654321/17861Test
رقم الانضمام: edsbas.FDF9C72A
قاعدة البيانات: BASE