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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Calcium signaling in single peripheral sensory nerve terminals.
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Calcium signaling in single peripheral sensory nerve terminals.

机译：单个周围感觉神经末梢中的钙信号传导。

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摘要

Peripheral sensory nerve terminals (PSNTs) have a dual function: reporting normal and abnormal sensations and releasing trophic factors to maintain the structure and function of epithelial cells. Although it is widely considered that intracellular Ca2+ plays a critical signaling role for both functions, the role of Ca2+ signaling has never been studied in PSNTs, primarily because of their small size and anatomical inaccessibility. Here, using epifluoresence microscopy and a fluorescent Ca2+ indicator, we report that action potentials or chemical irritation can elicit transient rises in [Ca2+]i (Ca2+ transients) in PSNTs within the corneal epithelium of the rat. In vitro electrical stimulation of the ciliary nerves in the eye, or electrical field stimulation of the cornea, evoked Ca2+ transients with a magnitude that was proportional to the number of stimuli applied over the range of 1-10 stimuli. Ca2+ transients were significantly blocked by 1 mm lidocaine, 4.1 microm saxitoxin (STX), or L-type Ca2+ channel antagonists (1 mm diltiazem or 20 microm nifedipine). The nociceptive agonist capsaicin (1 microm) elicited Ca2+ transients in all nerve terminals studied. Capsaicin-evoked Ca2+ transients were completely blocked by the vanilloid receptor 1 antagonist capsazepine (100 microm). In contrast, capsaicin-evoked Ca2+ transients were not attenuated by preincubation with 4.1 microm STX or 20 microm nifedipine. These findings demonstrate, for the first time, that nerve impulses or chemical stimulation promote Ca2+ entry into PSNTs, including nociceptors.
机译：周围感觉神经末梢（PSNT）具有双重功能：报告正常和异常的感觉并释放营养因子以维持上皮细胞的结构和功能。尽管人们普遍认为细胞内Ca2 +在这两种功能中都起着至关重要的信号作用，但由于PSNTs的体积小且解剖学上难以接近，因此尚未在PSNT中对其作用进行研究。在这里，我们使用表荧光显微镜和荧光Ca2 +指示剂，报告了动作电位或化学刺激可引起大鼠角膜上皮内PSNTs中[Ca2 +] i（Ca2 +瞬变）的瞬时升高。眼内睫状神经的体外电刺激或角膜的电场刺激可引起Ca2 +瞬变，其幅度与在1-10个刺激范围内施加的刺激数量成比例。 Ca2 +瞬变被1mm利多卡因，4.1微米沙西毒素（STX）或L型Ca2 +通道拮抗剂（1mm地尔硫卓或20微米硝苯地平）显着阻断。伤害性激动剂辣椒素（1微米）在研究的所有神经末梢均引起Ca2 +瞬变。辣椒素诱发的Ca2 +瞬变被类香草醇受体1拮抗剂卡塞平（100 microm）完全阻断。相反，通过与4.1微米STX或20微米硝苯地平进行预温育，辣椒素诱发的Ca2 +瞬变不会减弱。这些发现首次表明，神经冲动或化学刺激促进Ca2 +进入PSNT（包括伤害感受器）。

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