Modulatory effects and afferent pathway of gastric electric stimulation (GES) on spinal neurons receiving inputs from stomach in rats

GES has been suggested as therapy for patients with obesity or gastric motility disorders. The aim of this study was to investigate the spinal mechanism of GES effects on gastric function. Extracellular potentials of single spinal (T9–T10) neurons were recorded in pentobarbital anesthetized, paralyzed, ventilated male rats (n=19). Gastric distension (GD) was produced by air inflation of a balloon. One pair of platinum electrodes (1.0–1.5 cm apart) was sutured onto the serosal surface of the lesser curvature of the stomach. GES with four sets of parameters was applied for one minute: GES‐A (6 mA, 0.3 ms, 40 Hz, 2s on, 3s off), GES‐B (6 mA, 0.3 ms, 14 Hz, 0.1s on, 3s off), GES‐C (6 mA, 3 ms, 40 Hz, 2s on, 3s off), GES‐D (6 mA, 200 ms, 12 pulses/min). 61/157 (39%) spinal neurons responded to GD (20 and/or 60 mmHg, 20s). Most GD‐responsive neurons (n=47) were excitatory; the remainder was inhibitory (n=10) or excitatory‐inhibitory (n=4). GES‐A, ‐B, ‐C and –D affected activity of 32%, 16%, 78% and 35% of GD‐responsive neurons, respectively. Bilateral cervical vagotomy did not significantly alter effects of GES on 6/6 neurons. Resiniferatoxin (2.0 μg/kg, i.v.), an ultrapotent agonist of vanilloid receptor‐1, abolished neuronal responses to GD and effect of GES in 4/4 rats. The results suggested that GES mainly had an excitatory effect on T9–T10 spinal neurons with gastric inputs; neuronal response to GES was strengthened with stimulation at an increased pulse width and/or number of pulses. The modulatory effect of GES involved thoracic spinal (sympathetic) afferent fibers containing vanilloid receptor‐1. (Supported by OCAST)