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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Braga M F, Anderson A J, Harvey A L, Rowan E G

Department of Physiology and Pharmacology, University of Strathclyde, Glasgow.

Br J Pharmacol. 1992 May;106(1):91-4. doi: 10.1111/j.1476-5381.1992.tb14298.x.

In mouse triangularis sterni nerve-muscle preparations, reduced extracellular Na+ concentrations and low concentrations of the Na+ channel blocking toxins tetrodotoxin (TTX, 18-36 nM) and mu-conotoxin GIIIB (0.4-2.0 microM) selectively decreased the amplitude of the component of perineural waveforms associated with nerve terminal K+ currents, without affecting the main Na+ spike. 2. Intracellular recording of endplate potentials (e.p.ps) and miniature endplate potentials (m.e.p.ps) from triangularis sterni preparations revealed that TTX and mu-conotoxin GIIIB depressed the evoked quantal release of acetylcholine without significant effects on m.e.p.p. amplitude, frequency or time constant of decay. 3. The apparent block of K+ current by low concentrations of TTX and mu-conotoxin is probably not a direct effect on K+ channels but results from a decrease in the passive depolarization of nerve terminals following blockade of a small proportion of axonal Na+ channels.

在小鼠胸骨甲状肌神经-肌肉标本中，降低细胞外钠离子浓度以及使用低浓度的钠离子通道阻断毒素河豚毒素（TTX，18 - 36 nM）和芋螺毒素GIIIB（0.4 - 2.0 microM），可选择性降低与神经末梢钾离子电流相关的神经周波形成分的幅度，而不影响主要的钠离子峰电位。2. 对胸骨甲状肌标本进行终板电位（e.p.ps）和微小终板电位（m.e.p.ps）的细胞内记录显示，TTX和芋螺毒素GIIIB抑制乙酰胆碱的诱发量子释放，而对m.e.p.p.的幅度、频率或衰减时间常数无显著影响。3. 低浓度的TTX和芋螺毒素对钾离子电流的明显阻断可能不是对钾离子通道的直接作用，而是由于一小部分轴突钠离子通道被阻断后神经末梢被动去极化的减少所致。

Braga M F, Anderson A J, Harvey A L, Rowan E G

Department of Physiology and Pharmacology, University of Strathclyde, Glasgow.

Br J Pharmacol. 1992 May;106(1):91-4. doi: 10.1111/j.1476-5381.1992.tb14298.x.

In mouse triangularis sterni nerve-muscle preparations, reduced extracellular Na+ concentrations and low concentrations of the Na+ channel blocking toxins tetrodotoxin (TTX, 18-36 nM) and mu-conotoxin GIIIB (0.4-2.0 microM) selectively decreased the amplitude of the component of perineural waveforms associated with nerve terminal K+ currents, without affecting the main Na+ spike. 2. Intracellular recording of endplate potentials (e.p.ps) and miniature endplate potentials (m.e.p.ps) from triangularis sterni preparations revealed that TTX and mu-conotoxin GIIIB depressed the evoked quantal release of acetylcholine without significant effects on m.e.p.p. amplitude, frequency or time constant of decay. 3. The apparent block of K+ current by low concentrations of TTX and mu-conotoxin is probably not a direct effect on K+ channels but results from a decrease in the passive depolarization of nerve terminals following blockade of a small proportion of axonal Na+ channels.

在小鼠胸骨甲状肌神经-肌肉标本中，降低细胞外钠离子浓度以及使用低浓度的钠离子通道阻断毒素河豚毒素（TTX，18 - 36 nM）和芋螺毒素GIIIB（0.4 - 2.0 microM），可选择性降低与神经末梢钾离子电流相关的神经周波形成分的幅度，而不影响主要的钠离子峰电位。2. 对胸骨甲状肌标本进行终板电位（e.p.ps）和微小终板电位（m.e.p.ps）的细胞内记录显示，TTX和芋螺毒素GIIIB抑制乙酰胆碱的诱发量子释放，而对m.e.p.p.的幅度、频率或衰减时间常数无显著影响。3. 低浓度的TTX和芋螺毒素对钾离子电流的明显阻断可能不是对钾离子通道的直接作用，而是由于一小部分轴突钠离子通道被阻断后神经末梢被动去极化的减少所致。