Resetting Intrinsic Purinergic Modulation of Neural Activity: An Associative Mechanism?
Resetting Intrinsic Purinergic Modulation of Neural Activity: An Associative Mechanism?
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重置神经活动的内在嘌呤能调节：一种关联机制？
DOI：
10.1523/jneurosci.22-23-10461.2002
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发表时间：
2002
期刊：
影响因子：
--
通讯作者：
N. Dale
中科院分区：
文献类型：
--
作者：
N. Dale
嘌呤，ATP和腺苷，控制着非洲爪蟾胚胎游泳的停止和终止。这种内在的嘌呤能调节，必然存在于每一个游泳事件中，可能导致刻板的不灵活的行为，从而可能危及胚胎的存活。为了探索这种控制系统是否能表现出适应性，我使用了一个最小的模拟，其中模型神经元释放ATP，ATP（1）抑制K+电流，（2）被外核苷酸酶转化为腺苷，然后抑制Ca 2+电流。该模型神经元表现出由ATP和腺苷控制的调节性锋电位序列。上游代谢物ADP对将AMP转化为腺苷的外-5 ′-核苷酸酶的前馈抑制引入了适应性，并允许锋电位调节的重置。前馈抑制的强度决定了重置可能发生的程度。我已经通过在真实的胚胎中观察游泳来检验这些预测。以类似于单神经元模型预测的方式重置游泳的下降。通过阻断嘌呤受体，我证明了胚胎中的重置归因于嘌呤的作用，并且是腺苷产生的前馈抑制的结果。在运动系统中的rundown的重置可以被重新表述为一种关联机制，其中两个刺激的时间重合可以延长网络活动，如果它们落在特定的时间窗口内。时间窗的长度和神经活动延长的幅度都取决于前馈ADP介导的外-5 ′-核苷酸酶抑制的强度。
The purines, ATP and adenosine, control the rundown and termination of swimming in the Xenopus embryo. This intrinsic purinergic modulation, unavoidably present during every swimming episode, could lead to stereotyped inflexible behavior and consequently could jeopardize the survival of the embryo. To explore whether this control system can exhibit adaptability, I have used a minimal simulation in which a model neuron released ATP that (1) inhibited K+ currents and (2) was converted by ectonucleotidases to adenosine, which then inhibited Ca2+ currents. The model neuron exhibited an accommodating spike train controlled by the actions of ATP and adenosine. Feedforward inhibition by the upstream metabolite ADP of the ecto-5′-nucleotidase that converts AMP to adenosine introduced adaptability and allowed the resetting of spike accommodation. The strength of feedforward inhibition determined the extent to which resetting could occur. I have tested these predictions by examining swimming in the real embryo. The rundown of swimming was reset in a manner similar to that predicted by the single-neuron model. By blocking the purinoceptors, I have demonstrated that resetting in the embryo is attributable to the actions of the purines and results from feedforward inhibition of adenosine production. The resetting of rundown in the motor systems can be reformulated as an associative mechanism in which the temporal coincidence of two stimuli can prolong network activity if they fall within a particular time window. The length of the time window and the magnitude of the prolongation of neural activity both depend on the strength of the feedforward ADP-mediated inhibition of the ecto-5′-nucleotidase.
影响因子：
56.9
作者：
Porkka-Heiskanen, T;Strecker, RE;McCarley, RW
通讯作者：
McCarley, RW