Gastrointestinal extracellular recordings have been a core technique in motility research for a century. However, the bioelectrical basis of extracellular data has recently been challenged by claims that these techniques preferentially assay movement artifacts, cannot reproduce the underlying slow wave kinetics, and misrepresent the true slow wave frequency. These claims motivated this joint experimental–theoretical study, which aimed to define the sources and validity of extracellular potentials. In vivo extracellular recordings and video capture were performed in the porcine jejunum, before and after intra-arterial nifedipine administration. Gastric extracellular recordings were recorded simultaneously using conventional serosal contact and suction electrodes, and biphasic and monophasic extracellular potentials were simulated in a biophysical model. Contractions were abolished by nifedipine, but extracellular slow waves persisted, with unchanged amplitude, downstroke rate, velocity, and downstroke width (P > 0.10 for all), at reduced frequency (24% lower; P= 0.03). Simultaneous suction and conventional serosal extracellular recordings were identical in phase (frequency and activation–recovery interval), but varied in morphology (monophasic vs. biphasic; downstroke rate and amplitude: P < 0.0001). Simulations demonstrated the field contribution of current flow to extracellular potential and quantified the effects of localised depolarisation due to suction pressure on extracellular potential morphology. In sum, these results demonstrate that gastrointestinal extracellular slow wave recordings cannot be explained by motion artifacts, and are of a bioelectrical origin that is highly consistent with the underlying biophysics of slow wave propagation. Motion suppression is shown to be unnecessary as a routine control in in vivo extracellular studies, supporting the validity of the extant gastrointestinal extracellular literature.
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机译：胃肠道细胞外记录已经成为一个世纪以来动力研究的核心技术。但是，细胞外数据的生物电基础近来受到以下主张的挑战：这些技术优先分析运动伪影，无法再现潜在的慢波动力学，并且曲解了真实的慢波频率。这些主张激发了这项联合实验理论研究的目的，旨在确定细胞外电位的来源和有效性。在动脉内硝苯地平给药之前和之后，在猪空肠中进行体内细胞外记录和视频捕获。使用常规的浆膜接触和吸引电极同时记录胃外细胞记录，并在生物物理模型中模拟双相和单相细胞外电位。硝苯地平消除了收缩，但细胞外慢波持续存在，振幅，下冲程速率，速度和下冲程宽度均不变（所有P> 0.10），且频率降低（降低24％； P = 0.03）。同时吸气和常规浆膜细胞外记录的相位相同（频率和激活-恢复间隔），但形态各异（单相与双相；下冲程频率和幅度：P <0.0001）。模拟显示了电流对细胞外电位的场效应，并量化了由于抽吸压力对细胞外电位形态造成的局部去极化的影响。总之，这些结果表明胃肠道细胞外慢波记录不能用运动伪影来解释，并且是生物电起源，与慢波传播的潜在生物物理学高度一致。在体内细胞外研究中，显示出运动抑制作为常规控制是不必要的，这支持了现有胃肠道细胞外文献的有效性。
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