Long-term activity-dependent plasticity of action potential propagation delay and amplitude in cortical networks.

Long-term activity-dependent plasticity of action potential propagation delay and amplitude in cortical networks.
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皮质网络中的长期活性依赖性塑性势能延迟和幅度。

DOI:
10.1371/journal.pone.0002088
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发表时间:
2008-05-07
期刊:
影响因子:
3.7
通讯作者:
Potter SM
Potter SM
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Bakkum DJ;Chao ZC;Potter SM

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神经元动作电位在时间上的精确控制对于调节许多脑功能至关重要。从神经元的角度来看,其突触伙伴的动作电位传入输入的特定时间决定了该神经元是否以及何时发射自己的动作电位。调整这种输入将提供一种强大的机制来调节神经元的功能,进而调节大脑的功能。然而,动作电位计时的轴突可塑性与传统的稳定传播观念相悖,也与关注突触功效的活动依赖可塑性的主流理论相悖。在这里,我们展示了动作电位传播延迟的活动依赖性可塑性(几分钟后可达4 ms或40%,几小时后可达13 ms或74%)和振幅(高达87%)的发生。我们使用多电极阵列来诱导、检测和跟踪多个神经元在体外控制的新皮层网络中适应不同模式刺激时的传播变化。当阻断嗜离子性gabaergic和glutamergic受体时,重复同样的刺激不会发生这种变化。尽管动作电位的时间和幅度的变化的诱导依赖于突触传递,但这些变化的表达在突触受体阻滞剂存在时仍然存在。我们的结论是,随着突触效能的变化,传播可塑性提供了一种细胞机制来调节体外神经元网络功能,并可能在大脑中调节学习和记忆。
The precise temporal control of neuronal action potentials is essential for regulating many brain functions. From the viewpoint of a neuron, the specific timings of afferent input from the action potentials of its synaptic partners determines whether or not and when that neuron will fire its own action potential. Tuning such input would provide a powerful mechanism to adjust neuron function and in turn, that of the brain. However, axonal plasticity of action potential timing is counter to conventional notions of stable propagation and to the dominant theories of activity-dependent plasticity focusing on synaptic efficacies. Here we show the occurrence of activity-dependent plasticity of action potential propagation delays (up to 4 ms or 40% after minutes and 13 ms or 74% after hours) and amplitudes (up to 87%). We used a multi-electrode array to induce, detect, and track changes in propagation in multiple neurons while they adapted to different patterned stimuli in controlled neocortical networks in vitro. The changes did not occur when the same stimulation was repeated while blocking ionotropic gabaergic and glutamatergic receptors. Even though induction of changes in action potential timing and amplitude depended on synaptic transmission, the expression of these changes persisted in the presence of the synaptic receptor blockers. We conclude that, along with changes in synaptic efficacy, propagation plasticity provides a cellular mechanism to tune neuronal network function in vitro and potentially learning and memory in the brain.
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