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合成ω-芋螺毒素对突触传递的影响。

Effects of synthetic omega-conotoxin on synaptic transmission.

作者信息

Koyano K, Abe T, Nishiuchi Y, Sakakibara S

出版信息

Eur J Pharmacol. 1987 Mar 31;135(3):337-43. doi: 10.1016/0014-2999(87)90683-2.

Abstract

The effects of chemically synthesized omega-conotoxin GVIA (a neurotoxic peptide from Conus geographus) on synaptic transmission at the bullfrog sympathetic ganglion, frog neuromuscular junction and electric organ of the ray, Narke japonica, were studied. The synthetic toxin irreversibly suppressed synaptic transmission at these synapses by arresting the release of transmission from the nerve terminals without showing postsynaptic effects. This action of the toxin was effectively antagonized by high concentrations of extracellular Ca2+. The synthetic toxin irreversibly blocked the Ca2+-dependent action potential of bullfrog sympathetic ganglion cells. These results suggest that omega-conotoxin GVIA blocks synaptic transmission by interfering with the Ca2+ influx through the voltage-sensitive Ca2+ channel of the nerve terminal. These results indicate that the chemically synthesized omega-conotoxin GVIA acts exactly like the natural omega-conotoxin GVIA. Thus, the synthetic toxin can be used in place of the natural toxin as a useful probe for the voltage-sensitive Ca2+ channel in the nervous system.

摘要

研究了化学合成的ω-芋螺毒素GVIA(一种来自地纹芋螺的神经毒性肽)对牛蛙交感神经节、青蛙神经肌肉接头以及日本单鳍电鳐电器官突触传递的影响。合成毒素通过阻止神经末梢释放递质,不可逆地抑制了这些突触处的突触传递,且未表现出突触后效应。高浓度的细胞外Ca2+可有效拮抗毒素的这一作用。合成毒素不可逆地阻断了牛蛙交感神经节细胞依赖Ca2+的动作电位。这些结果表明,ω-芋螺毒素GVIA通过干扰Ca2+经神经末梢电压敏感性Ca2+通道内流来阻断突触传递。这些结果表明,化学合成的ω-芋螺毒素GVIA的作用与天然ω-芋螺毒素GVIA完全相同。因此,合成毒素可替代天然毒素,作为神经系统中电压敏感性Ca2+通道的有用探针。

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