Rapid exocytosis and endocytosis in nerve terminals of the rat posterior pituitary
Rapid exocytosis and endocytosis in nerve terminals of the rat posterior pituitary
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DOI：
10.1113/jphysiol.1996.sp021512
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发表时间：
1996-07-15
影响因子：
5.5
通讯作者：
Jackson, MB
中科院分区：
文献类型：
--
作者：
Hsu, SF;Jackson, MB
1.通过测量从大鼠垂体后叶制备的切片中电压钳位肽能神经末梢的膜电容，研究了Ca2+诱导的胞吐和胞吞2。去极化脉冲产生的电容迅速增加。随着电压的变化，这些增加与Ca2+电流平行变化。Ca2+电流的消除阻断了去极化引起的电容变化.去极化引起的电容变化随脉冲持续时间增加。电容的变化也增加了整合的Ca2+内流，但饱和在高水平的Ca2+进入。这种饱和允许我们估计190个囊泡的池大小，假设每个囊泡具有1 fF的电容。来自该池的囊泡以0.43 s的时间常数融合。电容变化随钙离子注入量的增大而增大.实验与简短的脉冲揭示了一个快速的组成部分，胞吐包括一个池的四十个囊泡，融合的时间常数为14毫秒。这个快速的过程可能反映了最终的Ca2+调节的触发步骤，这是不同的较慢的动力学步骤揭示了较长的持续时间的脉冲。较慢的步骤可能反映了囊泡在胞吐之前的引发。去极化诱导的电容增加，在大多数情况下，随后由电容的快速衰减，反映膜再摄取紧密耦合到胞吐。一个变量的快速内吞随后去极化诱导的电容增加。快速内吞至基线的时间常数为0.44 s。偶尔观察到过量的内吞作用，电容衰减低于预刺激基线，时间常数为2.1秒。快速内吞作用是缓慢的脉冲后，产生更大的增加细胞内Ca2+，细胞内Ca2+抑制快速内吞作用的假设一致。7.胞吐作用发生在去极化之后，没有可检测到的延迟，表明Ca2+触发神经末梢分泌神经肽的动力学与在其他快速分泌系统中观察到的动力学相当。
1. Ca2+-induced exocytosis and endocytosis were studied by measuring the membrane capacitance of voltage-clamped peptidergic nerve terminals in slices prepared from the rat posterior pituitary2. Depolarizing pulses produced rapid increases in capacitance. These increases varied in parallel with Ca2+ current as voltage was varied. Elimination of Ca2+ current blocked depolarization-induced capacitance changes.3. Depolarization-induced capacitance changes increased with pulse duration. Capacitance changes also increased wit integrated Ca2+ influx, but saturated at high levels of Ca2+ entry. This saturation allowed us to estimate a pool size of 190 vesicles, assuming each vesicle has a capacitance of 1 fF. Vesicles from this pool fused with a time constant of 0.43 s. The capacitance change increased with the fil st power of integrated Ca2+ influx.4. Experiments with briefer pulses revealed a rapid component of exocytosis comprising a pool of forty vesicles that fuse with a time constant of 14 ms. This rapid process may reflect a final Ca2+-regulated triggering step, which is distinct from the slower kinetic step revealed by longer duration pulses. The slower step may reflect a priming of vesicles prior to exocytosis.5. Depolarization-induced capacitance increases in most cases were followed by a rapid decay in capacitance, reflecting membrane reuptake tightly coupled to exocytosis. A variable amount of rapid endocytosis followed depolarization-induced capacitance increases. Tile time constant for rapid endocytosis to baseline was 0.44 s. Excess endocytosis was occasionally observed, with capacitance decaying below the pre-stimulus baseline with a time constant of 2.1 s.6. Rapid endocytosis was slower after pulses that produced greater increases in intracellular Ca2+, consistent with the hypothesis that intracellular Ca2+ inhibits rapid endocytosis. 7. Exocytosis follows depolarization with no detectable delay, indicating that Ca2+ triggers neuropeptide secretion from nerve terminals with kinetics comparable to that observed in other rapidly secreting systems.