In the hippocampus, the excitatory synapse between dentate granule cell axons - or mossy fibers (MF) - and CA3 pyramidal cells (MF-CA3) expresses robust forms of short-term plasticity, such as frequency facilitation and post-tetanic potentiation (PTP). These forms of plasticity are due to increases in neurotransmitter release, and can be engaged when dentate granule cells fire in bursts (e.g. during exploratory behaviors) and bring CA3 pyramidal neurons above threshold. While frequency facilitation at this synapse is limited by endogenous activation of presynaptic metabotropic glutamate receptors, whether MF-PTP can be regulated in an activity-dependent manner is unknown. Here, using physiologically relevant patterns of mossy fiber stimulation in acute mouse hippocampal slices, we found that disrupting postsynaptic Ca2+ dynamics increases MF-PTP, strongly suggesting a form of Ca2+-dependent retrograde suppression of this form of plasticity. PTP suppression requires a few seconds of MF bursting activity and Ca2+ release from internal stores. Our findings raise the possibility that the powerful MF-CA3 synapse can negatively regulate its own strength not only during PTP-inducing activity typical of normal exploratory behaviors, but also during epileptic activity.

中文翻译：

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在长满苔藓的纤维-CA3锥体细胞突触的强直后增强逆行抑制。

在海马中，齿状颗粒细胞轴突-或苔藓纤维（MF）-与CA3锥体细胞（MF-CA3）之间的兴奋性突触表现出强大的短期可塑性形式，例如频率促进和强直后增强（PTP） 。这些形式的可塑性是由于神经递质释放的增加所致，当齿状颗粒细胞突然爆发时（例如在探索行为中）并使CA3锥体神经元超过阈值时，可被利用。虽然该突触的频率促进受到突触前代谢型谷氨酸受体的内源性激活的限制，但尚不清楚MF-PTP是否可以以活性依赖性方式调节。在这里，我们使用急性鼠海马切片中苔藓纤维刺激的生理相关模式，发现破坏突触后Ca2 +动力学会增加MF-PTP，有力地暗示了这种形式的可塑性的一种依赖于Ca2 +的逆行抑制。PTP抑制需要几秒钟的MF爆发活动和内部存储中Ca2 +的释放。我们的发现增加了这样的可能性，即强大的MF-CA3突触不仅可以​​在正常探索行为典型的PTP诱导活动中而且可以在癫痫活动中负调节自身的力量。