Information processing and memory formation in the brain relies on release of the main excitatory neurotransmitter glutamate from presynaptic axonal specialisations. The classical Hebbian paradigm of synaptic memory, long-term potentiation (LTP) of transmission, has been widely associated with an increase in the postsynaptic receptor current. Whether and to what degree LTP induction also enhances presynaptic glutamate release has been the subject of debate. Here, we took advantage of the recently developed genetically encoded optical sensors of glutamate (iGluSnFR) to monitor its release at CA3-CA1 synapses in acute hippocampal slices, before and after the induction of LTP. We attempted to trace release events at multiple synapses simultaneously, by using two-photon excitation imaging in fast frame-scanning mode. We thus detected a significant increase in the average iGluSnFR signal during potentiation, which lasted for up to 90 min. This increase may reflect an increased amount of released glutamate or, alternatively, reduced glutamate binding to high-affinity glutamate transporters that compete with iGluSnFR.

中文翻译：

---

对多个突触原位的谷氨酸释放进行光学监控，可检测LTP诱导后的变化。

大脑中的信息处理和记忆形成依赖于突触前轴突专业的主要兴奋性神经递质谷氨酸的释放。突触记忆的经典Hebbian范式，即传输的长期增强（LTP），已与突触后受体电流的增加广泛相关。LTP诱导是否以及在何种程度上也能增强突触前谷氨酸的释放一直是争论的主题。在这里，我们利用最近开发的遗传编码的谷氨酸光学传感器（iGluSnFR）来监控LTP诱导前后在急性海马切片中CA3-CA1突触中的释放。我们试图通过在快速帧扫描模式下使用双光子激发成像来同时追踪多个突触的释放事件。因此，我们在增强过程中检测到平均iGluSnFR信号显着增加，持续了长达90分钟。这种增加可能反映了释放的谷氨酸盐数量增加，或者谷氨酸盐与与iGluSnFR竞争的高亲和力谷氨酸盐转运蛋白的结合减少。