Buchert-Rau B, Sonnhof U
Pflugers Arch. 1982 Jul;394(1):1-11. doi: 10.1007/BF01108300.
The action of Co2+ on the isolated frog spinal cord was studied by extracellular application of the ion in the superfusing solution. A complete and reversible blockade of chemical synaptic transmission by Co2+ (3 mmol/l) could be achieved after a superfusion period of 20-30 min. During continued Co2+ application (greater than 60 min) the following effects upon the motoneuron membrane, dorsal root and ventral root fibres were observed. Motoneurons and ventral root fibers: 1. prolongation of initial segment action potential to a maximum of 30 ms, 2. blockade of the long afterhyperpolarization, 3. abolition of adaptation, 4. increased duration of fibre action potential in the ventral root, 5. backfiring after ventral root stimulation. Dorsal root fibres: 1. prolongation of the extraspinal fibre action potential, 2. marked prolongation of the action potential of the terminal region, 3. backfiring of multiple action potentials after dorsal root stimulation. Even in the presence of Co2+, when synaptic transmission was completely blocked, strong convulsive reactions of the isolated spinal cord were observed. Intracellular injection of Co2+ into motoneurons did not affect the action potential, but led to a shift of the EIPSP towards the membrane potential. The results indicate that the induction of convulsive reactions by Co2+ is mainly due to a prolongation of action potentials. The plateau-like deformation of the action potential of the initial segment membrane and presumably of the terminal region of nerve endings results in retrograde propagation of action potentials and in some cases induces oscillatory discharge of single neurons.
通过在灌流液中细胞外施加离子,研究了Co2+对离体青蛙脊髓的作用。在灌流20 - 30分钟后,Co2+(3 mmol/l)可实现对化学突触传递的完全可逆性阻断。在持续施加Co2+(大于60分钟)期间,观察到对运动神经元膜、背根和腹根纤维有以下影响。运动神经元和腹根纤维:1. 起始段动作电位延长至最长30毫秒;2. 长时超极化后电位阻断;3. 适应性消失;4. 腹根中纤维动作电位持续时间增加;5. 腹根刺激后出现逆向放电。背根纤维:1. 脊髓外纤维动作电位延长;2. 终末区域动作电位显著延长;3. 背根刺激后多个动作电位逆向放电。即使在存在Co2+且突触传递完全阻断的情况下,仍观察到离体脊髓有强烈的惊厥反应。向运动神经元内注射Co2+不影响动作电位,但导致兴奋性突触后电位向膜电位方向偏移。结果表明,Co2+诱导惊厥反应主要是由于动作电位延长。起始段膜以及可能还有神经末梢终末区域动作电位的平台样变形导致动作电位逆向传播,在某些情况下诱导单个神经元的振荡性放电。