Pfizer KCL Pain Labs, Wolfson Centre for Age-Related Diseases, King's College London, London, United Kingdom ; Pfizer Global R&D, Sandwich, United Kingdom.
PLoS One. 2013 Nov 20;8(11):e80722. doi: 10.1371/journal.pone.0080722. eCollection 2013.
Pathological changes in axonal function are integral features of many neurological disorders, yet our knowledge of the molecular basis of axonal dysfunction remains limited. Microfluidic chambers (MFCs) can provide unique insight into the axonal compartment independent of the soma. Here we demonstrate how an MFC based cell culture system can be readily adapted for the study of axonal function in vitro. We illustrate the ease and versatility to assay electrogenesis and conduction of action potentials (APs) in naïve, damaged or sensitized DRG axons using calcium imaging at the soma for pharmacological screening or patch-clamp electrophysiology for detailed biophysical characterisation. To demonstrate the adaptability of the system, we report by way of example functional changes in nociceptor axons following sensitization by neurotrophins and axotomy in vitro. We show that NGF can locally sensitize axonal responses to capsaicin, independent of the soma. Axotomizing neurons in MFC results in a significant increase in the proportion of neurons that respond to axonal stimulation, and interestingly leads to accumulation of Nav1.8 channels in regenerating axons. Axotomy also augmented AP amplitude following axotomy and altered activation thresholds in a subpopulation of regenerating axons. We further show how the system can readily be used to study modulation of axonal function by non-neuronal cells such as keratinocytes. Hence we describe a novel in vitro platform for the study of axonal function and a surrogate model for nerve injury and sensitization.
轴突功能的病理性改变是许多神经疾病的固有特征,但我们对轴突功能障碍的分子基础的了解仍然有限。微流控室(MFC)可以为轴突区室提供独立于胞体的独特见解。在这里,我们展示了如何轻松地将基于 MFC 的细胞培养系统适应体外轴突功能的研究。我们说明了使用钙成像在胞体上进行药物筛选或膜片钳电生理学进行详细的生物物理特性分析,轻松而灵活地检测未受损、受损或致敏的 DRG 轴突中的电发生和动作电位(AP)传导的方法。为了证明该系统的适应性,我们通过示例报告了神经营养因子敏化和体外轴突切断后伤害感受器轴突的功能变化。我们表明,NGF 可以局部敏化轴突对辣椒素的反应,而与胞体无关。在 MFC 中切断神经元会导致对轴突刺激有反应的神经元比例显著增加,有趣的是,这会导致 Nav1.8 通道在再生轴突中积累。轴突切断还会增加轴突切断后的 AP 幅度,并改变再生轴突中一部分的激活阈值。我们进一步展示了如何轻松地将该系统用于研究非神经元细胞(如角质形成细胞)对轴突功能的调节。因此,我们描述了一种用于研究轴突功能的新型体外平台,以及用于神经损伤和致敏的替代模型。