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首页> 外文期刊>Lancet Neurology >Synaptic plasticity in the ischaemic brain.
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Synaptic plasticity in the ischaemic brain.

机译:缺血性脑中的突触可塑性。

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摘要

Activity-dependent long-term potentiation (LTP) of excitatory neurotransmission underlies specific forms of associative learning and memory. A brief period of energy deprivation induces LTP in specific subsets of neurons; this synaptic plasticity might contribute to the delayed effects of brain ischaemia. In this review, we discuss the similarities and differences between LTP induced by energy deprivation and physiological pathological plasticity induced by energy deprivation can play a part in delayed neuronal death in the hippocampus and the striatum after global ischaemia and in the conversion of ischaemic penumbra to infarct core after focal ischaemia. We discuss evidence that ischaemia could also induce protective and reparative forms of neuronal plasticity that may play a part in ischaemic tolerance and poststroke recovery.
机译:兴奋性神经传递的活动依赖性长期增强(LTP)是联想学习和记忆的特定形式的基础。短暂的能量剥夺会在神经元的特定亚群中诱导LTP。这种突触可塑性可能会导致脑缺血的延迟效应。在这篇综述中,我们讨论了由能量剥夺引起的LTP与能量剥夺引起的生理病理可塑性之间的异同可以在整体缺血后海马和纹状体的延迟神经元死亡以及缺血性半影​​向梗死的转化中起作用局部缺血后的核心。我们讨论的证据表明,缺血还可能诱导保护性和修复性的神经元可塑性,可能在缺血耐受性和中风后恢复中发挥作用。

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