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机译:ERK1 / 2介导的BDNF-TRKB信号传导的破坏导致突触损伤导致氟化物诱导的发育神经毒性有助于
Department of Environmental Health MOE Key Lab of Environment and Health School of Public Health;
Department of Environmental Health MOE Key Lab of Environment and Health School of Public Health;
Department of Environmental Health MOE Key Lab of Environment and Health School of Public Health;
Department of Environmental Health MOE Key Lab of Environment and Health School of Public Health;
Department of Environmental Health MOE Key Lab of Environment and Health School of Public Health;
Department of Environmental Health MOE Key Lab of Environment and Health School of Public Health;
Department of Environmental Health MOE Key Lab of Environment and Health School of Public Health;
Department of Environmental Health MOE Key Lab of Environment and Health School of Public Health;
Department of Environmental Health MOE Key Lab of Environment and Health School of Public Health;
Department of Environmental Health MOE Key Lab of Environment and Health School of Public Health;
Fluoride; Developmental neurotoxicity; Synaptic impairment; BDNF–TrkB signaling; Phospho–ERK1/2;
机译:ERK1 / 2介导的BDNF-TRKB信号传导的破坏导致突触损伤导致氟化物诱导的发育神经毒性有助于
机译:钙调蛋白依赖性蛋白激酶IIα/脑源性神经营养因子(α-CaMKII/ BDNF)信号的破坏与锌缺乏引起的认知和突触可塑性受损有关。
机译:钙调蛋白依赖性蛋白激酶IIα/脑源性神经营养因子(α-CaMKII/ BDNF)信号的破坏与锌缺乏引起的认知和突触可塑性损害相关
机译:BDNF诱导的皮层神经元突触传递的增强
机译:TrkB介导的信号转导减少导致神经肌肉突触结构改变,神经传递受损和肌肉无力
机译:金雀异黄素通过调节cAMP / CREB和BDNF-TrkB-PI3K / Akt信号传导减弱异氟烷诱导的神经毒性并改善受损的空间学习和记忆能力
机译:Genistein衰减异氟烷诱导的神经毒性,通过调节CAMP / CREB和BDNF-TRKB-PI3K / AKT信号传导来提高空间学习和记忆受损