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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Excessive release of (3H) noradrenaline by veratridine and ischemia in spinal cord.
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Excessive release of (3H) noradrenaline by veratridine and ischemia in spinal cord.

机译：Veratridine和脊髓缺血导致（3H）去甲肾上腺素过度释放。

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摘要

In this study, the properties of ischemic condition-induced and veratridine-evoked [3H]noradrenaline ([3H]NA) release from rat spinal cord slices were compared. It was expected that ischemia mimicked by oxygen and glucose deprivation results in the impairment of Na+/K+ -ATPase with a consequent elevation of the intracellular Na+ -level which reverses the NA carrier and promotes excessive NA release, and veratridine, by the activation of Na+ channels, releases NA both carrier-mediated and Ca2+ -dependent, i.e. vesicular manner. In our experiments, veratridine (1-100 microM) dose-dependently increased the resting [3H]NA release, and its effect was only partially blocked by low temperature or the lack of external calcium, whereas the sodium channel inhibitor tetrodotoxin (TTX, 1 microM) completely prevented it, indicating that veratridine induces NA release via axonal depolarization and reversing the transporters by eliciting Na+ -influx. In contrast to TTX, the local anesthetic lidocaine (100 microM) only partially blocked the veratridine-induced [3H]NA release due to its inhibitory action on K+ channels. The ischemia-induced [3H]NA release was abolished at 12 degrees C, a temperature known to block only the transporter-mediated release of transmitters. However, lidocaine was also partially effective to reverse the action of ischemia on the NA release, indicating that lidocaine is not a useful compound in the treatment of spinal cord-injured patients against the excessive excytotoxic NA release.
机译：在这项研究中，比较了缺血性条件诱发的和藜芦碱诱发的[3H]去甲肾上腺素（[3H] NA）从大鼠脊髓切片中释放的特性。预期通过氧和葡萄糖剥夺模拟的局部缺血会导致Na + / K + -ATPase受损，从而导致细胞内Na +-水平升高，从而逆转NA载体并促进Na +的活化，并通过激活Na +来促进维拉替尼的生长。通道，释放NA的载体介导和Ca 2 +依赖，即水泡的方式。在我们的实验中，维他命（1-100 microM）剂量依赖性地增加了静止的[3H] NA释放，其作用仅被低温或缺乏外部钙部分阻止，而钠通道抑制剂河豚毒素（TTX，1 microM）完全阻止了它的发生，这表明维拉替丁可通过轴突去极化诱导NA释放，并通过引起Na +流入而逆转转运蛋白。与TTX相比，局部麻醉剂利多卡因（100 microM）由于其对K +通道的抑制作用，仅部分阻断了藜芦啶诱导的[3H] NA释放。缺血诱导的[3H] NA释放在12°C时被取消，该温度已知仅阻断转运蛋白介导的递质释放。但是，利多卡因在逆转缺血对NA释放的作用方面也部分有效，表明利多卡因不是治疗脊髓损伤的患者的过度细胞毒性NA释放的有用化合物。

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