title: Gastric electrical stimulation decreases gastric distension-induced central nociception response through direct action on primary afferents.
abstract: OBJECTIVE
  Gastric 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.
  
  
  METHODS
  Gastric 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.
  
  
  RESULTS
  GES 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.
  
  
  CONCLUSIONS
  GES decreases GD-induced pain and/or discomfort likely through a direct modulation of gastric spinal afferents reducing central processing of visceral nociception.
authors.affiliation: Nutrition, Gut & Brain Unit (ADEN - INSERM U1073), Institute for Biomedical Research and innovation, Rouen University, Rouen, France.
authors.forename: Wassila
authors.initials: W
authors.lastname: Ouelaa
authors.forename: Ibtissem
authors.initials: I
authors.lastname: Ghouzali
authors.forename: Ludovic
authors.initials: L
authors.lastname: Langlois
authors.forename: Serguei
authors.initials: S
authors.lastname: Fetissov
authors.forename: Pierre
authors.initials: P
authors.lastname: Déchelotte
authors.forename: Philippe
authors.initials: P
authors.lastname: Ducrotté
authors.forename: Anne Marie
authors.initials: AM
authors.lastname: Leroi
authors.forename: Guillaume
authors.initials: G
authors.lastname: Gourcerol
mesh_terms: D000344:Afferent Pathways; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D001794:Blood Pressure; D004599:Electric Stimulation Therapy; D005727:Ganglia, Spinal / Q000473:pathology / Q000503:physiopathology; D008297:Male; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism; D059225:Nociception / Q000502:physiology*; D010146:Pain / Q000150:complications; D010286:Paraventricular Hypothalamic Nucleus / Q000473:pathology / Q000503:physiopathology; D010766:Phosphorylation; D020671:Posterior Horn Cells / Q000378:metabolism; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017552:Solitary Nucleus / Q000473:pathology / Q000503:physiopathology; D013272:Stomach Diseases / Q000150:complications / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy*
chemical_list: D015415:Biomarkers; D016760:Proto-Oncogene Proteins c-fos; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3