[Show abstract][Hide abstract] ABSTRACT: 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.
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.
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).
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.
[Show abstract][Hide abstract] ABSTRACT: The study aims to find the effect of motilin on neuronal activity of gastric distension-responsive neurons in rat hippocampus and its possible mechanism. Single unit discharges in the hippocampal CA1 region were recorded extracellularly by means of four-barrel glass micropipettes in anesthetized rats and the expression of nNOS in hippocampus was observed by fluo-immunohistochemistry staining. Of the 171 recorded neurons, 76.0% were GD-excitatory (GD-E) neurons and 24.0% were GD-inhibited (GD-I) neurons. The 57.6% of GD-E neurons showed an excitatory response to motilin and the same effect was observed in 51.7% GD-I neurons. However, when NOS inhibitor nitro-l-arginine methyl ester (l-NAME) was administrated previously, the followed motilin-induced excitatory responsiveness of GD-responsive neurons was reduced. In contrast, discharge activity of GD-responsive neurons with motilin was enhanced by pretreatment of NO precursor l-arginine. The expression of nNOS-IR positive neurons was significantly increased in CA1 after administration of motilin. Our findings suggested that motilin excited the GD-responsive neurons in the hippocampal CA1 region and the excitatory effect of motilin may be mediated by the endogenous NO.