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Transsynaptic modulation of presynaptic short-term plasticity induction in hippocampal mossy fiber synapses
bioRxiv - Neuroscience Pub Date : 2020-10-25 , DOI: 10.1101/2020.10.25.353953
David Vandael , Yuji Okamoto , Peter Jonas

The hippocampal mossy fiber synapse is a key synapse of the trisynaptic circuit of the hippocampus. Post-tetanic potentiation (PTP) is the most powerful form of plasticity at this synaptic connection. It is widely believed that mossy fiber PTP is an entirely presynaptic phenomenon, implying that PTP induction is input-specific, and requires neither activity of multiple inputs nor stimulation of postsynaptic neurons for induction. Thus, mossy fiber PTP appears to lack cooperativity and associativity that characterize other forms of plasticity. To directly test these predictions, we made paired recordings between single mossy fiber terminals and postsynaptic CA3 pyramidal neurons in rat brain slices. By stimulating parallel but non-overlapping mossy fiber bouton (MFB) inputs converging onto single CA3 neurons, we confirmed that PTP was input specific and non-cooperative. Unexpectedly, mossy fiber PTP showed anti-associative induction properties. Mossy fiber excitatory postsynaptic currents (EPSCs) showed only minimal PTP after combined pre- and postsynaptic high frequency stimulation (HFS) with intact postsynaptic Ca2+ signaling (0.1 mM EGTA), but marked PTP in the absence of postsynaptic spiking and after suppression of postsynaptic Ca2+ signaling (10 mM EGTA). PTP was rescued by blocking Ca2+ entry via voltage-gated R-type and to a smaller extent L-type Ca2+ channels. PTP was also recovered by extracellular application of group II metabotropic glutamate receptor (mGluR) antagonists and vacuolar-type (v-type) H+-ATPase inhibitors, suggesting the involvement of retrograde vesicular glutamate signaling. Transsynaptic regulation of PTP induction may increase the computational power of mossy fiber synapses, and implement a break on hippocampal mossy fiber detonation.

中文翻译:

海马苔藓纤维突触突触前短期可塑性诱导的突触调制。

海马苔藓纤维突触是海马三突触回路的关键突触。破伤风后增强(PTP)是这种突触连接的最强大的可塑性形式。普遍认为,生苔纤维PTP是一种完全的突触前现象,这意味着PTP诱导是输入特异性的,既不需要多次输入的活动,也不需要刺激突触后神经元进行诱导。因此,长满苔藓的纤维PTP似乎缺乏其他形式可塑性的协同性和缔合性。为了直接检验这些预测,我们在大鼠脑切片中的单个苔藓纤维末端和突触后CA3锥体神经元之间进行了配对记录。通过刺激会聚到单个CA3神经元上的平行但不重叠的苔藓纤维钮扣(MFB)输入,我们确认PTP是特定于输入且不合作的。出乎意料的是,长满苔藓的纤维PTP表现出抗缔合诱导特性。苔藓纤维兴奋性突触后电流(EPSC)在突触前和突触后高频率刺激(HFS)结合完整的突触后Ca2 +信号(0.1 mM EGTA)后仅显示出最小的PTP,但在没有突触后尖峰和抑制突触后Ca2 +后标记为PTP信号(10 mM EGTA)。通过阻止Ca2 +通过电压门控R型通道和较小程度的L型Ca2 +通道进入,可以挽救PTP。通过在细胞外应用II组代谢型谷氨酸受体(mGluR)拮抗剂和液泡型(v型)H + -ATPase抑制剂也可恢复PTP,表明参与了逆行囊泡谷氨酸信号传导。
更新日期:2020-10-27
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