Habermann E
Naunyn Schmiedebergs Arch Pharmacol. 1981 Dec;318(2):105-11. doi: 10.1007/BF00508834.
Tetanus toxin and, to a lesser degree, botulinum A toxin partially depress the basal and the potassium evoked outflow of [3H]noradrenaline from preloaded particulate rat forebrain cortex. The effect is due to the toxins and not to any contaminant, as shown by dialysis, heating and antitoxin treatment, and also by replacement of crystalline botulinum A toxin with purified neurotoxin. Tetanus toxin also depresses the outflow due to sea anemone toxin II, 4-aminopyridine and d-amphetamine. The effect of the toxins proceeds with time and strongly depends on temperature. Once manifest the tetanus toxin effect is not reversed by antitoxin. Pretreatment with V. cholerae neuraminidase degrades the long-chain gangliosides quantitatively to GM1. Tetanus toxin, applied subsequently remains fully active. High concentrations of tetanus toxin and botulinum A neurotoxin promote the outflow of small amounts of tritium within short incubation times. It is concluded: a) Tetanus toxin is a broad range neurotoxin which acts on processes subsequent to the depolarization step. b) Long-chain gangliosides are only binding sites, but not receptors of tetanus toxin. c) Botulinum A toxin is less potent but resembles tetanus toxin in both promoting and depressing the outflow of noradrenaline.
破伤风毒素以及在较小程度上肉毒杆菌A毒素能部分抑制预先加载放射性标记的去甲肾上腺素从大鼠前脑皮层微粒体中基础状态下和钾离子诱发的流出。透析、加热和抗毒素处理以及用纯化的神经毒素替代结晶状肉毒杆菌A毒素的实验均表明，该作用是由毒素引起，而非任何污染物所致。破伤风毒素还能抑制由海葵毒素II、4-氨基吡啶和右旋苯丙胺引起的去甲肾上腺素流出。毒素的作用随时间推移而进行，且强烈依赖于温度。一旦破伤风毒素的作用显现，抗毒素无法将其逆转。用霍乱弧菌神经氨酸酶预处理可将长链神经节苷脂定量降解为GM1。随后施加的破伤风毒素仍保持完全活性。高浓度的破伤风毒素和肉毒杆菌A神经毒素在短时间孵育内会促进少量氚的流出。得出以下结论：a）破伤风毒素是一种作用于去极化步骤之后过程的广谱神经毒素。b）长链神经节苷脂仅是破伤风毒素的结合位点，而非受体。c）肉毒杆菌A毒素效力较弱，但在促进和抑制去甲肾上腺素流出方面与破伤风毒素相似。
