Cerebellar stellate cells (CSCs) are spontaneously active, tonically firing (5-30 Hz), inhibitory interneurons that synapse onto Purkinje cells. We previously analyzed the excitability properties of CSCs, focusing on four key features: type I excitability, non-monotonic first-spike latency, switching in responsiveness and runup (i.e., temporal increase in excitability during whole-cell configuration). In this study, we extend this analysis by using whole-cell configuration to show that these neurons can also burst when treated with certain pharmacological agents separately or jointly. Indeed, treatment with (4-Aminopyridine) 4-AP, a partial blocker of delayed rectifier and A-type K⁺ channels, at low doses induces a bursting profile in CSCs significantly different than that produced at high doses or when it is applied at low doses but with cadmium (Cd²⁺), a blocker of high voltage-activated (HVA) Ca²⁺ channels. By expanding a previously revised Hodgkin–Huxley type model, through the inclusion of Ca²⁺-activated K⁺ (K(Ca)) and HVA currents, we explain how these bursts are generated and what their underlying dynamics are. Specifically, we demonstrate that the expanded model preserves the four excitability features of CSCs, as well as captures their bursting patterns induced by 4-AP and Cd²⁺. Model investigation reveals that 4-AP is potentiating HVA, inducing square-wave bursting at low doses and pseudo-plateau bursting at high doses, whereas Cd²⁺ is potentiating K(Ca), inducing pseudo-plateau bursting when applied in combination with low doses of 4-AP. Using bifurcation analysis, we show that spike adding in square-wave bursts is non-sequential when gradually changing HVA and K(Ca) maximum conductances, delayed Hopf is responsible for generating the plateau segment within the active phase of pseudo-plateau bursts, and bursting can become “chaotic” when HVA and K(Ca) maximum conductances are made low and high, respectively. These results highlight the secondary effects of the drugs applied and suggest that CSCs have all the ingredients needed for bursting.

小脑星状细胞（CSC）是自发活跃的，具有音调的（5-30 Hz）抑制性神经元，可突触到Purkinje细胞上。我们先前分析了CSC的兴奋性属性，着重于四个关键特征：I型兴奋性，非单调的第一峰值潜伏期，响应性和启动时间的切换（即，全细胞配置期间兴奋性的暂时增加）。在这项研究中，我们通过使用全细胞配置扩展了此分析，以显示当使用某些药理学药物单独或联合治疗时，这些神经元也会破裂。的确，使用（4-氨基吡啶）4-AP（延迟整流剂和A型K ⁺低剂量通道引起的CSC爆裂曲线与高剂量或在低剂量但使用镉（Cd 2 ⁺）（高电压激活（HVA）Ca ²⁺通道的阻滞剂）时产生的爆裂曲线显着不同。通过包含Ca ²⁺激活的K ⁺（K（Ca））和HVA电流，通过扩展先前修订的Hodgkin-Huxley型模型，我们解释了这些猝发是如何产生的以及其潜在的动力学是什么。具体而言，我们证明了扩展模型保留了CSC的四个兴奋性特征，并捕获了由4-AP和Cd ²⁺引起的爆裂模式。。模型研究表明4-AP增强HVA，在低剂量下诱导方波爆发，在高剂量下诱导假高原爆发，而Cd ²⁺增强K（Ca），与低剂量联合应用时诱导假高原爆发。剂量的4-AP。使用分叉分析，我们显示，当逐渐改变HVA和K（Ca）最大电导时，方波猝发中的尖峰添加是不连续的，延迟的Hopf负责在伪高原猝发的活动相中生成高原段，当分别使HVA和K（Ca）最大电导变低和变高时，爆裂可能会变得“混乱”。这些结果突出了所用药物的次要作用，并表明CSC具有爆破所需的所有成分。