Vavoulis Dimitris V, Nikitin Eugeny S, Kemenes Ildikó, Marra Vincenzo, Feng Jianfeng, Benjamin Paul R, Kemenes György
Department of Computer Science, University of Warwick Coventry, UK.
Front Behav Neurosci. 2010 May 5;4:19. doi: 10.3389/fnbeh.2010.00019. eCollection 2010.
The Cerebral Giant Cells (CGCs) are a pair of identified modulatory interneurons in the Central Nervous System of the pond snail Lymnaea stagnalis with an important role in the expression of both unconditioned and conditioned feeding behavior. Following single-trial food-reward classical conditioning, the membrane potential of the CGCs becomes persistently depolarized. This depolarization contributes to the conditioned response by facilitating sensory cell to command neuron synapses, which results in the activation of the feeding network by the conditioned stimulus. Despite the depolarization of the membrane potential, which enables the CGGs to play a key role in learning-induced network plasticity, there is no persistent change in the tonic firing rate or shape of the action potentials, allowing these neurons to retain their normal network function in feeding. In order to understand the ionic mechanisms of this novel combination of plasticity and stability of intrinsic electrical properties, we first constructed and validated a Hodgkin-Huxley-type model of the CGCs. We then used this model to elucidate how learning-induced changes in a somal persistent sodium and a delayed rectifier potassium current lead to a persistent depolarization of the CGCs whilst maintaining their firing rate. Including in the model an additional increase in the conductance of a high-voltage-activated calcium current allowed the spike amplitude and spike duration also to be maintained after conditioning. We conclude therefore that a balanced increase in three identified conductances is sufficient to explain the electrophysiological changes found in the CGCs after classical conditioning.
脑巨细胞(CGCs)是椎实螺中枢神经系统中一对已被确认的调节性中间神经元,在无条件和条件性摄食行为的表达中发挥重要作用。在单次试验食物奖励经典条件反射后,CGCs的膜电位会持续去极化。这种去极化通过促进感觉细胞与指令神经元之间的突触传递,对条件反应产生作用,进而导致条件刺激激活摄食网络。尽管膜电位去极化使CGGs在学习诱导的网络可塑性中发挥关键作用,但动作电位的持续发放率或形状并无持续变化,从而使这些神经元在摄食过程中能够保持其正常的网络功能。为了理解这种可塑性与内在电特性稳定性新组合的离子机制,我们首先构建并验证了CGCs的霍奇金-赫胥黎型模型。然后,我们利用该模型阐明学习诱导的体细胞持续性钠电流和延迟整流钾电流变化如何导致CGCs持续去极化,同时维持其发放率。在模型中加入高压激活钙电流电导的额外增加,使得条件反射后动作电位的幅度和持续时间也能得以维持。因此,我们得出结论,三种已确认电导的平衡增加足以解释经典条件反射后CGCs中发现的电生理变化。