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Dear Editor,

We thank Dr. Nakayama for his acknowledgment that movement can be a significant artifact in extracellular recordings of biopotentials. In our article1 we showed that gastric movements are not slow monophasic events as described by Dr. Nakayama. We tracked small dots affixed to the gastric serosa to understand the movement trajectories that might influence an electrode against the surface. With each contractile cycle, the dots moved in a complex orbits, changing direction repeatedly. These tiny movements correlated with and created relatively large artifacts in electrical recordings and are likely to be the main source of the spiky electrical records, not Ca2+ currents or action potentials.

In fact, much of the gastric musculature does not experience Ca2+ action potentials, even during stimulation by agonists,2 Our intracellular electrical recording from mice confirm these findings.1 We also used wortmannin, a myosin light chain kinase inhibitor, to suppress movement that does not affect currents flowing across cell membranes (resting membrane potentials and slow waves were unaffected by wortmannin). Wortmannin also blocked biopotentials, strengthening the conclusion that extracellular potentials recorded by surface electrodes are largely movement artifacts.

Proper filtering is important, and we agree that filtering affects the waveforms recorded by extracellular techniques. We initially chose bandpass characteristics like those used by Professor William Lammers in his many studies of GI biopotentials.3 In contrast we also sampled between (0.3–100 Hz),1 and this did not affect our results or interpretations. The main signal one expects to record from stomach would result from rapid, large changes in membrane potential that occur during slow wave upstrokes (>1 V s−1 when recording intracellularly from interstitial cells of Cajal (ICC); cells that generate and actively propagate slow waves). The upstroke mechanism is analogous to the Na+ current of cardiac action potentials. In ECGs the QRS (representing the action potential upstroke) is resolved with greatest amplitude and signal to noise ratio. Gastric slow waves are far slower in rise-time (about 100-fold) and far smaller in amplitude (about half) than cardiac action potentials, and in the bowel only ICC actively regenerate slow waves. So only a fraction of cells in the gut (<10%) are active current sources generating field potentials. Low pass filtering <1 Hz would attenuate fast changes in potential during slow waves, and this would attenuate the signals most likely to be resolved by extracellular recording. Our findings make it clear that careful suppression of movement is an essential control for experiments employing extracellular electrical recording.

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No competing interests declared.

References

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