Enhancement of antral contractions and vagal afferent signaling with synchronized electrical stimulation

Abstract

Gastric filling activates vagal afferents involved in peripheral signaling to the central nervous system (CNS) for food intake. It is not known whether these afferents linearly encode increasing contractions of the antrum during antral distension (AD). The aim of this study was to investigate effects of AD and electrically enhanced antral contractions on responses of vagal afferents innervating the antrum. Single-fiber recordings were made from the vagal afferents in anesthetized male Long-Evans rats. Antral contractions were measured with a solid-state probe placed in the antrum. A nonexcitatory electrical stimulation (NES) inducing no smooth muscle contractions was applied during the ascending phase of antral contractions to enhance subsequent antral contractions. Fifty-six fibers identified during AD (1 ml for 30 s) were studied through different types of mechanical stimuli. Under normal conditions, one group of fibers exhibited rhythmic firing in phase with antral contractions. Another group of fibers had nonrhythmic spontaneous firing. Responses of 15 fibers were tested with NES during multiple-step distension (MSD). NES produced a mean increase in antral contraction amplitude (177.1 +/- 35.3%) and vagal afferent firing (21.6 +/- 2.6%). Results show that both passive distension and enhanced antral contractions activate distension-sensitive vagal afferents. Responses of these fibers increase linearly to enhanced antral contraction induced by NES or MSD up to a distending volume of 0.6 ml. However, responses reached a plateau at a distending volume >0.8 ml. We concluded that enhanced contraction of the antrum can activate vagal afferents signaling to the CNS.

Systematic review: applications and future of gastric electrical stimulation

“…In another rodent study, vagal afferent fibres were activated when antral contractions were induced with GES. 59 …”

Modulatory effects and afferent pathways of gastric electrical stimulation on rat thoracic spinal neurons receiving input from the stomach

“…Using an advanced spectral analysis of heart rate variability for the assessment of vagal activity, GES is found to be involved with increased vagal activity and accelerated gastric emptying in dogs and rats (Liu et al 2004;Ouyang et al 2003). Additionally, GES is reported to produce an increase in the firing rate of vagal single afferent fibers associated with antral contractions of the stomach in rats (Peles et al 2003), and GES mainly exerts excitatory effects on NTS neuronal activity (Qin et al 2005). However, some investigators noted a role of sympathetic pathways in the effects of GES on gastrointestinal functions.…”

“…Previous studies using atropine and vagotomy in dogs have indicated that vagal afferent and/or efferent pathways are involved in the regulation of GES on gastric motility Grundfest-Bronaltowski et al 1990;Liu et al 2004;Ouyang et al 2003). In rats, GES can activate vagal afferent fibers innervating the stomach (Peles et al 2003) and modulate neuronal activity in the nucleus tractus solitarii, where vagal afferent fibers terminate (Qin et al 2005). A few recent studies suggest that the effects of GES with different parameters on gastric motility also involve the sympathetic nerve system.…”

Characterization of T9–T10 spinal neurons with duodenal input and modulation by gastric electrical stimulation in rats

“…For example, GES increases the firing rate of single vagal gastric afferent fibers and mainly exerts excitatory effects on neuronal activity in the nucleus tractus solitarii in rats (Peles et al 2003, Qin et al 2005. Vagotomy eliminates the anti-emetic effects of short-pulse GES on nausea and vomiting induced by vasopressin .…”

“…Effects of GES on gastric motility have been shown to involve vagal afferent and/or efferent pathways in dogs Grundfest-Bronaltowski et al 1990;Liu et al 2004;Ouyang et al 2003). In rats, GES can activate vagal afferent fibers innervating the stomach (Peles et al 2003) and modulate activity of neurons in the nucleus tractus solitarii receiving gastric vagal afferents (Qin et al 2005). A few recent studies further suggest that effects of GES with varying parameters on gastric motility involve the sympathetic alpha-and beta-adrenergic sympathetic efferent pathways system (Zhu and Chen 2005;Ouyang et al 2005).…”