Department of Physiology, McGill University, Montréal, QC, Canada.
Department of Pharmacology and Therapeutics, McGill University, Montréal, QC, Canada.
PLoS Comput Biol. 2020 Dec 14;16(12):e1008463. doi: 10.1371/journal.pcbi.1008463. eCollection 2020 Dec.
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.
小脑星形细胞(CSC)是自发活跃的、持续放电(5-30Hz)的抑制性中间神经元,与浦肯野细胞形成突触。我们之前分析了 CSC 的兴奋性特性,重点关注四个关键特征:I 型兴奋性、非单调的第一个峰潜伏期、反应性切换和上升(即在整个细胞构型期间兴奋性的时间增加)。在这项研究中,我们通过使用全细胞构型扩展了这一分析,表明这些神经元在单独或联合使用某些药物时也可以爆发。事实上,用 4-氨基吡啶(4-AP)处理,一种延迟整流和 A 型 K+通道的部分阻断剂,在低剂量下会导致 CSC 中产生显著不同于高剂量或在低剂量下应用时的爆发模式,或者当它与镉(Cd2+)一起应用时,一种高电压激活(HVA)Ca2+通道的阻断剂。通过扩展之前修订的 Hodgkin-Huxley 型模型,通过包含 Ca2+-激活的 K+(K(Ca))和 HVA 电流,我们解释了这些爆发是如何产生的,以及它们的潜在动力学是什么。具体来说,我们证明扩展模型保留了 CSC 的四个兴奋性特征,以及捕获由 4-AP 和 Cd2+诱导的爆发模式。模型研究表明,4-AP 增强 HVA,在低剂量下诱导方波爆发,在高剂量下诱导伪平台爆发,而 Cd2+增强 K(Ca),当与低剂量的 4-AP 联合应用时诱导伪平台爆发。通过分岔分析,我们表明在逐渐改变 HVA 和 K(Ca)最大电导时,方波爆发中的尖峰添加是非序列的,延迟的 Hopf 负责在伪平台爆发的活跃相内产生平台段,并且当 HVA 和 K(Ca)最大电导变得低和高时,爆发可以变得“混沌”。这些结果突出了应用药物的次要效应,并表明 CSC 具有爆发所需的所有成分。