Neurodegenerative disorders can exhibit'/> Loss of protohaem IX farnesyltransferase in mature dentate granule cells impairs short‐term facilitation at mossy fibre to CA3 pyramidal cell synapses
首页> 美国卫生研究院文献>The Journal of Physiology >Loss of protohaem IX farnesyltransferase in mature dentate granule cells impairs short‐term facilitation at mossy fibre to CA3 pyramidal cell synapses
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Loss of protohaem IX farnesyltransferase in mature dentate granule cells impairs short‐term facilitation at mossy fibre to CA3 pyramidal cell synapses

机译:成熟的齿状颗粒细胞中原血球IX法呢基转移酶的丧失削弱了生苔纤维对CA3锥体细胞突触的短期促进作用

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摘要

Key points class="unordered" style="list-style-type:disc" id="tjp12214-list-0001">Neurodegenerative disorders can exhibit dysfunctional mitochondrial respiratory chain complex IV activity.Conditional deletion of cytochrome c oxidase, the terminal enzyme in the respiratory electron transport chain of mitochondria, from hippocampal dentate granule cells in mice does not affect low‐frequency dentate to CA3 glutamatergic synaptic transmission.High‐frequency dentate to CA3 glutamatergic synaptic transmission and feedforward inhibition are significantly attenuated in cytochrome c oxidase‐deficient mice.Intact presynaptic mitochondrial function is critical for the short‐term dynamics of mossy fibre to CA3 synaptic function.
机译:关键点 class =“ unordered” style =“ list-style-type:disc” id =“ tjp12214-list-0001”> <!-list-behavior = unordered prefix-word = mark-type = disc max- label-size = 0-> 神经退行性疾病可表现出功能异常的线粒体呼吸链复合物IV活性。 有条件地删除了细胞色素c氧化酶,即线粒体呼吸电子运输链中的末端酶小鼠海马齿状颗粒细胞不影响低频齿状体对CA3谷氨酸能突触的传递。 高频齿状体对CA3谷氨酸能突触的传递和前馈抑制作用在细胞色素C氧化酶缺陷型小鼠中显着减弱。 / li> 完整的突触前线粒体功能对于生苔纤维对CA3突触功能的短期动力学至关重要。

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