Electrical resonance and Ca2+ influx in the synaptic terminal of depolarizing bipolar cells from the goldfish retina
Electrical resonance and Ca2+ influx in the synaptic terminal of depolarizing bipolar cells from the goldfish retina
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DOI：
10.1111/j.1469-7793.1997.571ba.x
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发表时间：
1997-12-15
影响因子：
5.5
通讯作者：
Lagnado, L
中科院分区：
文献类型：
--
作者：
Burrone, J;Lagnado, L
1.在从金鱼视网膜分离的去极化双极细胞中进行了全细胞记录和胞浆[Ca ~（2+）]的Fura-2测量。目的是研究突触终末钙内流的电压信号调节.电流-电压关系在约-44mV处呈线性。在该阈值下，注入1 pA电流触发维持的“全或无”去极化至-34 mV的平台，与输入电阻的降低和频率为50-70 Hz且初始振幅为4-10 mV的阻尼电压振荡相关。经常观察到5-10 Hz的第二频率分量。在少数细胞中，对电流注入的反应是短暂的，在下冲的情况下恢复。未受刺激的双极细胞产生类似的电压信号，由通过振幅连续变化的非特异性阳离子电导进入细胞的电流驱动。钙电流激活的阈值为-43 mV，突触终末游离[Ca ~（2+）]（i）在去极化反应期间升高。与膜标记FM 1 -43相关的荧光的同时测量表明，这些Ca 2+信号刺激胞吐作用。再生去极化和相关的[Ca 2 +]升高通过用30 μ M硝苯地平抑制L-型Ca 2+通道来阻断。除极电位超过-40 mV时，还可诱发外向整流钾电流。通过用Ba 2+替代外部Ca 2+来阻断该电流，导致去极化响应期间达到的电压增加至+10 mV。大部分的K+电流被100 nM的Charybdotoxin阻断，表明它是由大电导的Ca 2+激活的K+通道。瞬时电压门控的K+电流仍然存在，其在-40 mV时开始激活。高频电压振荡被100 nM的Charybdotoxin阻断，但低频振荡被阻断。这些结果表明，去极化双极细胞的电压响应是由L型Ca ~（2+）通道、Ca ~（2+）激活的K ~+通道和电压依赖性K ~+通道共同决定的。这种电导率的组合调节Ca 2+流入突触末端并赋予双极细胞电共振。
1. Whole-cell recordings and fura-2 measurements of cytoplasmic [Ca2+] were made in depolarizing bipolar cells isolated from the retinae of goldfish. The aim was to study the voltage signal that regulates Ca2+ influx in the synaptic terminal.2. The current-voltage relation was linear up to about -44 mV. At this threshold, the injection of 1 pA of current triggered a maintained 'all-or-none' depolarization to a plateau of -34 mV, associated with a decrease in input resistance and a damped voltage oscillation with a frequency of 50-70 Hz and initial amplitude of 4-10 mV. A second frequency component of 5-10 Hz was often observed. In a minority of cells the response to current injection was transient, recovering with an undershoot.3. Unstimulated bipolar cells generated similar voltage signals, driven by current entering the cell through a non-specific cation conductance that continuously varied in amplitude.4. The threshold for activation of the Ca2+ current was -43 mV and free [Ca2+](i) in the synaptic terminal rose during a depolarizing response. Simultaneous measurements of the fluorescence associated with the membrane marker FM1-43 demonstrated that these Ca2+ signals stimulated exocytosis. Regenerative depolarizations and associated rises in [Ca2+], were blocked by inhibiting L-type Ca2+ channels with 30 mu M nifedipine.5. Depolarization beyond -40 mV also elicited an outwardly rectifying K+ current. Blocking this current by replacing external Ca2+ with Ba2+ caused the voltage reached during a depolarizing response to increase to +10 mV.6. The majority of the K+ current was blocked by 100 nM charybdotoxin, indicating that it was carried by large-conductance Ca2+-activated K+ channels. a transient voltage-gated K+ current remained, which began to activate at -40 mV. High-frequency voltage oscillations were blocked by 100 nM charybdotoxin, but low-frequency oscillations remained.7. These results indicate that the voltage response of depolarizing bipolar cells is shaped by L-type Ca2+ channels, Ca2+-activated K+ channels and voltage-dependent K+ channels. This combination of conductaaances regulates Ca2+ influx into the synaptic terminal and confers an electrical resonance on the bipolar cell.