Calcium in sympathetic varicosities of mouse vas deferens during facilitation, augmentation and autoinhibition
Calcium in sympathetic varicosities of mouse vas deferens during facilitation, augmentation and autoinhibition
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DOI：
10.1111/j.1469-7793.1997.521bj.x
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发表时间：
1997-08-01
影响因子：
5.5
通讯作者：
Bennett, MR
中科院分区：
文献类型：
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作者：
Brain, KL;Bennett, MR
1.通过沿着节后神经的顺行运输，将钙指示剂Oregon Green 488 BAPTA-1装载到小鼠输精管的交感神经末梢。静脉曲张中钙浓度的变化 (Delta[Ca2+](v)) 是根据 5 Hz 的单脉冲、短（5 脉冲）和长（200 脉冲）序列确定的。2。所有静脉曲张均显示出对每个脉冲的显着 Delta[Ca2+](v) 响应。对于所有静脉曲张，升高的 Delta[Ca2+](v) 分两个阶段下降，具有相似的动力学：快速阶段（时间常数，0.42 +/- 0.05 s）和中度阶段（3.6 +/- 0.4 s）。3。线扫描共聚焦显微镜显示，静脉曲张间区域单脉冲后单个终端的Delta[Ca2+]小于静脉曲张区域。4．用 Cd2+（在无钙溶液中）阻断电压敏感钙通道，完全阻断刺激时的 Delta[Ca2+](v)。添加硝苯地平 (10 μM)、omega-芋螺毒素 GVIA (100 nM) 或 omega-agatoxin TK (100 nM) 表明 47 +/- 6% 的诱发反应是由 N 型钙通道介导的。5． Ryanodine (10 mu M) 不会显着改变响应短训练的 Delta[Ca2+](v) 幅度。6．在个体静脉曲张中观察到Delta[Ca2+](v)的自发增加，并且静脉曲张之间Delta[Ca2+](v)的增加是耦合的。7．突触前 α(2)-受体拮抗剂育亨宾 (10 μM) 使响应 5 个脉冲 (5 Hz) 的 Delta[Ca2+](v) 幅度增加 54 +/- 14%，而 α(2)-受体激动剂可乐定 (1 μM) 使 Delta[Ca2+](v) 降低 55 +/- 4%.8。这些结果根据以下假设进行讨论：伴随着促进和增强，交感神经末梢分泌的可能性增加是由于冲动后钙流入后残留的残留Delta[Ca2+](v)，并且去甲肾上腺素在突触前起作用，通过改变钙流入来降低分泌的可能性。
1. The sympathetic nerve terminals of the mouse vas deferens were loaded with the calcium indicator Oregon Green 488 BAPTA-1 by orthograde transport along the postganglionic nerves. Changes in the calcium concentration in the varicosity (Delta[Ca2+](v)) were determined following single impulses, and short (5-impulse) and long (200-impulse) trains at 5 Hz.2. All varicosities showed a significant Delta[Ca2+](v) in response to every single impulse. The elevated Delta[Ca2+](v) declined in two phases with similar kinetics for all varicosities: a fast phase (time constant, 0.42 +/- 0.05 s) and a moderate phase (3.6 +/- 0.4 s).3. Line scanning confocal microscopy revealed that the Delta[Ca2+] of a single terminal following single impulses was smaller for the intervaricose regions than for the varicosities.4. Blockade of the voltage-sensitive calcium channels with Cd2+ (in calcium-free solution) completely blocked the Delta[Ca2+](v) on stimulation. The addition of either nifedipine (10 mu M), omega-conotoxin GVIA (100 nM) or omega-agatoxin TK (100 nM) showed that 47 +/- 6% of the evoked response was mediated by N-type calcium channels.5. Ryanodine (10 mu M) did not significantly change the amplitude of Delta[Ca2+](v) in response to short trains.6. Spontaneous increases in Delta[Ca2+](v) were observed in individual varicosities, with coupling in the increase of Delta[Ca2+](v) between varicosities.7. The presynaptic alpha(2)-receptor antagonist yohimbine (10 mu M) increased the amplitude of Delta[Ca2+](v) in response to five impulses (5 Hz) by 54 +/- 14%, while the alpha(2)-receptor agonist clonidine (1 mu M) decreased the Delta[Ca2+](v) by 55 +/- 4%.8. These results are discussed in terms of the hypotheses that the increased probability for secretion at sympathetic nerve terminals which accompanies facilitation and augmentation is due to the residual Delta[Ca2+](v) remaining after the calcium influx following impulses and that noradrenaline acts presynaptically to decrease the probability of secretion by modifying calcium influx.