Tegnér J, Lansner A, Grillner S
Department of Neuroscience, Nobel Institute for Neurophysiology, Karolinska Institutet, Stockholm, Sweden.
J Comput Neurosci. 1998 May;5(2):121-40. doi: 10.1023/a:1008897031013.
It is crucial to determine the effects on the network level of a modulation of intrinsic membrane properties. The role calcium-dependent potassium channels, KCa, in the lamprey locomotor system has been investigated extensively. Earlier experimental studies have shown that apamin, which affects one type of KCa, increases the cycle duration of the locomotor network, due to effects on the burst termination. The effects of apamin were here larger when the network had a low level of activity (burst frequency 0.5 to 1 Hz) as compared to a higher rate (> 2 Hz). By using a previously developed simulation model based on the lamprey locomotor network, we show that the model could account for the frequency dependence of the apamin modulation, if only the KCa conductance activated by Ca2+ entering during the action potential was altered and not the KCa conductance activated by Ca2+ entering through NMDA channels. The present simulation model of the spinal network in the lamprey can thus account for earlier experimental results with apamin on the network and cellular level that previously appeared enigmatic.
确定内在膜特性调制对网络水平的影响至关重要。钙依赖性钾通道（KCa）在七鳃鳗运动系统中的作用已得到广泛研究。早期的实验研究表明，影响一种KCa的蜂毒明肽会增加运动网络的周期时长，这是由于对爆发终止的影响。与较高频率（>2 Hz）相比，当网络活动水平较低（爆发频率为0.5至1 Hz）时，蜂毒明肽在此处的影响更大。通过使用先前基于七鳃鳗运动网络开发的模拟模型，我们表明，如果仅改变动作电位期间Ca2+进入所激活的KCa电导，而不改变通过NMDA通道进入的Ca2+所激活的KCa电导，该模型就能解释蜂毒明肽调制的频率依赖性。因此，目前七鳃鳗脊髓网络的模拟模型可以解释早期关于蜂毒明肽在网络和细胞水平上的实验结果，这些结果之前显得很神秘。
