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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

Heppner T J, Fiekers J F

Department of Anatomy and Neurobiology, University of Vermont College of Medicine, Burlington 05405.

Comp Biochem Physiol C Comp Pharmacol Toxicol. 1992 Jun;102(2):335-8. doi: 10.1016/0742-8413(92)90121-m.

The effects of VX (10 microM) were examined on sympathetic ganglion neurons from the bullfrog using intracellular recording techniques. 2. VX significantly increased the amplitude of the residual EPSP from 4.8 +/- 0.86 mV (n = 4) to 13.7 +/- 1.23 mV (n = 4). 3. VX significantly decreased the membrane potential 5.2 +/- 0.75 mV (n = 6). The input resistance and the duration of the spike afterhyperpolarization (AHP) were also reduced 69.8% and 69.6% of control, respectively. 4. VX increased neuronal excitability greater than 200% (n = 5) of control. 5. The VX-induced neuronal excitability may result from a reduction in the duration of the AHP and contribute to the CNS toxicity.

使用细胞内记录技术，研究了VX（10微摩尔）对牛蛙交感神经节神经元的影响。2. VX使残余兴奋性突触后电位（EPSP）的幅度从4.8±0.86毫伏（n = 4）显著增加到13.7±1.23毫伏（n = 4）。3. VX使膜电位显著降低5.2±0.75毫伏（n = 6）。输入电阻和动作电位后超极化（AHP）的持续时间也分别降低至对照的69.8%和69.6%。4. VX使神经元兴奋性比对照增加超过200%（n = 5）。5. VX诱导的神经元兴奋性可能是由于AHP持续时间缩短所致，并导致中枢神经系统毒性。

Heppner T J, Fiekers J F

Department of Anatomy and Neurobiology, University of Vermont College of Medicine, Burlington 05405.

Comp Biochem Physiol C Comp Pharmacol Toxicol. 1992 Jun;102(2):335-8. doi: 10.1016/0742-8413(92)90121-m.

The effects of VX (10 microM) were examined on sympathetic ganglion neurons from the bullfrog using intracellular recording techniques. 2. VX significantly increased the amplitude of the residual EPSP from 4.8 +/- 0.86 mV (n = 4) to 13.7 +/- 1.23 mV (n = 4). 3. VX significantly decreased the membrane potential 5.2 +/- 0.75 mV (n = 6). The input resistance and the duration of the spike afterhyperpolarization (AHP) were also reduced 69.8% and 69.6% of control, respectively. 4. VX increased neuronal excitability greater than 200% (n = 5) of control. 5. The VX-induced neuronal excitability may result from a reduction in the duration of the AHP and contribute to the CNS toxicity.

使用细胞内记录技术，研究了VX（10微摩尔）对牛蛙交感神经节神经元的影响。2. VX使残余兴奋性突触后电位（EPSP）的幅度从4.8±0.86毫伏（n = 4）显著增加到13.7±1.23毫伏（n = 4）。3. VX使膜电位显著降低5.2±0.75毫伏（n = 6）。输入电阻和动作电位后超极化（AHP）的持续时间也分别降低至对照的69.8%和69.6%。4. VX使神经元兴奋性比对照增加超过200%（n = 5）。5. VX诱导的神经元兴奋性可能是由于AHP持续时间缩短所致，并导致中枢神经系统毒性。