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Ca2+ current facilitation determines short-term facilitation at inhibitory synapses between cerebellar Purkinje cells

机译:Ca2 +的当前促进作用决定了小脑浦肯野细胞之间抑制性突触的短期促进作用

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摘要

Short-term synaptic facilitation is critical for information processing of neuronal circuits. Several Ca2+-dependent positive regulations of transmitter release have been suggested as candidate mechanisms underlying facilitation. However, the small sizes of presynaptic terminals have hindered the biophysical study of short-term facilitation. In the present study, by directly recording from the axon terminal of a rat cerebellar Purkinje cell (PC) in culture, we demonstrate a crucial role of [Ca2+](i)-dependent facilitation of Ca2+ currents in short-term facilitation at inhibitory PC-PC synapses. Voltage clamp recording was performed from a PC axon terminal visualized by enhanced green fluorescent protein, and the Ca2+ currents elicited by the voltage command consisting of action potential waveforms were recorded. The amplitude of presynaptic Ca2+ current was augmented upon high-frequency paired-pulse stimulation in a [Ca2+](i)-dependent manner, leading to paired-pulse facilitation of Ca2+ currents. Paired recordings from a presynaptic PC axon terminal and a postsynaptic PC soma demonstrated that the paired-pulse facilitation of inhibitory synaptic transmission between PCs showed 4-5th power dependence on that of Ca2+ currents, and was completely abolished when the Ca2+ current amplitude was adjusted to be identical. Thus, short-term facilitation of Ca2+ currents predominantly mediates short-term synaptic facilitation at synapses between PCs.
机译:短期突触促进对神经元回路的信息处理至关重要。已经提出了几种依赖Ca 2+的递质释放的正调控作为促进促进作用的候选机制。然而,突触前末端的小尺寸阻碍了短期促进的生物物理研究。在本研究中,通过直接从培养物中的大鼠小脑浦肯野细胞(PC)的轴突末端记录,我们证明了Ca2 +电流的[Ca2 +](i)依赖性促进在抑制性PC的短期促进中的关键作用-PC突触。从通过增强的绿色荧光蛋白可视化的PC轴突端进行电压钳记录,并记录由动作电位波形组成的电压指令引起的Ca2 +电流。突触前Ca2 +电流的幅度在高频成对脉冲刺激下以[Ca2 +](i)依赖的方式增加,导致成对脉冲促进了Ca2 +电流。突触前PC轴突末端和突触后PC体的配对记录表明,成对脉冲促进PC之间抑制性突触传递的过程显示,其对Ca2 +电流的依赖性为4-5倍,而当将Ca2 +电流幅度调整为一样。因此,Ca 2+电流的短期促进主要在PC之间的突触中介导短期突触促进。

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