Abstract
Background & AimsGastric electrical stimulation (GES) is an effective therapy to treat patients with chronic dyspepsia refractory to medical management. However, its mechanisms of action remain poorly understood.MethodsGastric pain was induced by performing gastric distension (GD) in anesthetized rats. Pain response was monitored by measuring the pseudo-affective reflex (e.g., blood pressure variation), while neuronal activation was determined using c-fos immunochemistry in the central nervous system. Involvement of primary afferents was assessed by measuring phosphorylation of ERK1/2 in dorsal root ganglia.ResultsGES decreased blood pressure variation induced by GD, and prevented GD-induced neuronal activation in the dorsal horn of the spinal cord (T9–T10), the nucleus of the solitary tract and in CRF neurons of the hypothalamic paraventricular nucleus. This effect remained unaltered within the spinal cord when sectioning the medulla at the T5 level. Furthermore, GES prevented GD-induced phosphorylation of ERK1/2 in dorsal root ganglia.ConclusionsGES decreases GD-induced pain and/or discomfort likely through a direct modulation of gastric spinal afferents reducing central processing of visceral nociception.
Highlights
Over the past decade, gastric electrical stimulation (GES) has become a new therapeutic option for patients with medically refractory dyspeptic symptoms, including nausea and vomiting, epigastric pain, gastric fullness and early satiety [1,2,3,4,5,6,7,8,9]
We showed that GES could act on neurons of the hypothalamic paraventricular nucleus (PVN) to decrease corticotropin-releasing factor (CRF) transcript expression [14]
Gastric electrical stimulation decreases the variation of blood pressure in response to gastric distension
Summary
Gastric electrical stimulation (GES) has become a new therapeutic option for patients with medically refractory dyspeptic symptoms, including nausea and vomiting, epigastric pain, gastric fullness and early satiety [1,2,3,4,5,6,7,8,9]. We showed that GES could act on neurons of the hypothalamic paraventricular nucleus (PVN) to decrease corticotropin-releasing factor (CRF) transcript expression [14] This effect remained unaltered after subdiaphragmatic vagotomy, suggesting that spinal afferent pathway was likely to be involved. We assessed the effect of GES on gastric visceral sensitivity, and determined whether this effect recruited spinal primary afferents This was achieved by investigating the influence of GES on functional and molecular markers of pain response to gastric distension (GD) in a rat model.
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