Effects of Gastric Electric Stimulation on Gastric Distention Responsive Neurons and Expressions of CCK in Rodent Hippocampus

Objective: Gastric electrical stimulation (GES) has been introduced for treating obesity. The hippocampus is known to be involved in the regulation of gastrointestinal motility. Changes in hypathalumus cholecystokinin (CCK) have been observed in genetically obese rodents. This experiment was to study the effect of GES on the activities of neurons and the expression of CCK in the hippocampus. Methods and Procedures: We investigated the effect of GES (GES‐I: pulse train of standard parameters; GES‐2: reduced train‐on time; GES‐3: increased pulse width; GES‐4: reduced pulse frequency) on neurons responsive to gastric distention (GD) by recording extracellular potentials of single neurons and observing the expression of CCK in the rodent hippocampus by immunohistochemistry staining, radioimmunoassay, and real‐time PCR. Results: 92.1% of neurons in the CA2‐3 region responded to GD, 53.2% of which showed excitation (GD‐E), and 46.8% showed inhibition (GD‐I). 64.8% GD‐responsive neurons were excited by GES. The response was associated with stimulation strength, pulse width, and frequency; 70.6, 57.1, 94.4, and 66.7% of GD‐E and 72.7, 57.1, 86.4, and 50% of GD‐I neurons showed excitatory responses to GES‐I, −2, −3, and −4, respectively. CCK immunoreactive positive neurons (P < 0.001), the content of CCK‐like materials (P < 0.05) and the amount of CCK mRNA were significantly increased after GES (P < 0.05). Discussion: These findings suggest the central, neuronal, and hormonal mechanisms of GES. GES may excite the activity of GD‐sensitive neurons and increase the expression of CCK in the hippocampus. These excitatory effects of GES seem to be related to the parameters of stimulation.