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首页> 外文期刊>Neuron >Functional maturation of CA1 synapses involves activity-dependent loss of tonic kainate receptor-mediated inhibition of glutamate release.
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Functional maturation of CA1 synapses involves activity-dependent loss of tonic kainate receptor-mediated inhibition of glutamate release.

机译：CA1突触的功能成熟涉及依赖于活性的补剂红藻酸酯受体介导的谷氨酸释放抑制。

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摘要

Early in development, excitatory synapses transmit with low efficacy, one mechanism for which is a low probability of transmitter release (Pr). However, little is known about the developmental mechanisms that control activity-dependent maturation of the presynaptic release. Here, we show that during early development, transmission at CA3-CA1 synapses is regulated by a high-affinity, G protein-dependent kainate receptor (KAR), which is endogenously activated by ambient glutamate. By tonically depressing glutamate release, this mechanism sets the dynamic properties of neonatal inputs to favor transmission during high frequency bursts of activity, typical for developing neuronal networks. In response to induction of LTP, the tonic activation of KAR is rapidly down regulated, causing an increase in Pr and profoundly changing the dynamic properties of transmission. Early development of the glutamatergic connectivity thus involves an activity-dependent loss of presynaptic KAR function producing maturation in the mode of excitatory transmission from CA3 to CA1.
机译：在发展的早期，兴奋性突触的发射效率低，其机制之一是释放发射器（Pr）的可能性低。但是，关于控制活动依赖的突触前释放的成熟的发育机制知之甚少。在这里，我们表明，在早期发育过程中，CA3-CA1突触的传递受高亲和力，G蛋白依赖性海藻酸酯受体（KAR）调节，该受体被周围谷氨酸内源性激活。通过调节性抑制谷氨酸的释放，该机制设置了新生儿输入的动态特性，以促进高频活动爆发期间的传递，这对于发展神经元网络是典型的。响应于LTP的诱导，KAR的强直激活被迅速下调，导致Pr的增加并深刻改变了传输的动态特性。因此，谷氨酸能连接的早期发展涉及以活动性丧失突触前KAR功能，从而以从CA3到CA1的兴奋性传递方式成熟。

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