Kreger A S, Molgó J, Comella J X, Hansson B, Thesleff S
Medical Sciences Research Institute, Herndon, Virginia 22071.
Toxicon. 1993 Mar;31(3):307-17. doi: 10.1016/0041-0101(93)90148-c.
The neuromuscular toxicity of stonefish (Synanceia trachynis) venom was characterized by electrophysiological and electron microscopic examination of isolated murine and frog nerve-skeletal muscle preparations exposed to various concentrations of venom. Low concentrations of venom (2.5-10 micrograms/ml) acted presynaptically by causing release and depletion of neurotransmitter from the nerve terminal. The response was Na+ channel-independent (resistant to tetrodotoxin), required the presence of either Ca2+ or Mg2+, and was observed with botulinum neurotoxin-paralyzed nerve-muscle preparations. Higher concentrations of venom (100-300 micrograms/ml) acted postsynaptically and presynaptically. They caused irreversible depolarization of muscle cells and microscopically observable muscle and nerve damage. We conclude that the previously observed neuromuscular toxicity of stonefish venom is a consequence of the venom's dose-dependent, presynaptic and postsynaptic actions at the myoneural junction.
通过对暴露于不同浓度毒液的离体小鼠和青蛙神经 - 骨骼肌标本进行电生理和电子显微镜检查,对玫瑰毒鲉(Synanceia trachynis)毒液的神经肌肉毒性进行了表征。低浓度毒液(2.5 - 10微克/毫升)通过引起神经末梢神经递质的释放和耗竭,在突触前起作用。该反应不依赖于Na +通道(对河豚毒素有抗性),需要Ca2 +或Mg2 +的存在,并且在肉毒杆菌神经毒素麻痹的神经 - 肌肉标本中也可观察到。较高浓度的毒液(100 - 300微克/毫升)在突触后和突触前均起作用。它们导致肌肉细胞不可逆的去极化以及显微镜下可观察到的肌肉和神经损伤。我们得出结论,先前观察到的玫瑰毒鲉毒液的神经肌肉毒性是毒液在肌神经接头处剂量依赖性的突触前和突触后作用的结果。