首页> 外文期刊>The Journal of Physiology >Calcium in sympathetic varicosities of mouse vas deferens during facilitation, augmentation and autoinhibition.
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Calcium in sympathetic varicosities of mouse vas deferens during facilitation, augmentation and autoinhibition.

机译:促进,增强和自抑制过程中小鼠输精管交感性静脉曲张中的钙。

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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 microM), omega-conotoxinGVIA (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 microM) 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 microM) 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 microM) 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.
机译:1.通过沿神经节后神经原位运输,将钙指示剂Oregon Green 488 BAPTA-1加载到小鼠输精管的交感神经末梢。在单脉冲,5 Hz的短脉冲(5脉冲)和长脉冲(200脉冲)后,确定静脉曲张中钙浓度的变化(δ[Ca2 +] v)。 2.所有静脉曲张均显示出对每个单脉冲的显着变化[Ca2 +] v。对于所有静脉曲张,升高的δ[Ca2 +] v在两个阶段均以相似的动力学下降:快速阶段(时间常数为0.42 +/- 0.05 s)和中等阶段(3.6 +/- 0.4 s)。 3.线扫描共聚焦显微镜显示,单脉冲后单个末端的δ[Ca 2+]对于静脉曲张区域比对静脉曲张小。 4.用Cd2 +(在无钙溶液中)阻断压敏钙通道可完全阻断刺激后的[Ca2 +] v。硝苯地平(10 microM),ω-芋螺毒素GVIA(100 nM)或omega-毒素毒素TK(100 nM)的添加表明,诱发的反应的47 +/- 6%由N型钙通道介导。 5. Ryanodine(10 microM)响应短火车并没有显着改变δ[Ca2 +] v的幅度。 6.在各个静脉曲张中观察到δ[Ca2 +] v的自发增加,并且在静脉曲张之间出现了[Ca2 +] v的增加的耦合。 7.突触前的α2受体拮抗剂育亨宾(10 microM)响应五次脉冲(5 Hz),使[Ca2 +] v的幅度增加了54 +/- 14%,而α2受体激动剂可乐定(1 microM)将[Ca2 +] v降低了55 +/- 4%。 8.根据以下假设对这些结果进行了讨论:在促进和增强的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δ[Ca2 +] v残留,而去甲肾上腺素会先突通过改变钙质流入的分泌概率。

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