title: Experimental ulcers alter voltage-sensitive sodium currents in rat gastric sensory neurons.
abstract: OBJECTIVE
  Voltage-dependent Na+ currents are important determinants of excitability. We hypothesized that gastric inflammation alters Na+ current properties in primary sensory neurons.
  
  
  METHODS
  The stomach was surgically exposed in rats to inject the retrograde tracer 1.1'-dioctadecyl-3,3,3,'3-tetramethylindocarbocyanine methanesulfonate and saline (control) or 20% acetic acid (ulcer group) into the gastric wall. Nodose or thoracic dorsal root ganglia (DRG) were harvested after 7 days to culture neurons and record Na+ currents using patch clamp techniques.
  
  
  RESULTS
  There were no lesions in the control and 3 +/- 1 ulcers in the ulcer group. Na+ currents recovered significantly more rapidly from inactivation in nodose and DRG neurons obtained from animals in the ulcer group compared with controls. This was partially a result of an increase in the relative contribution of the tetrodotoxin-resistant to the peak sodium current. In addition, the recovery kinetics of the tetrodotoxin-sensitive current were faster. In DRG neurons, gastric inflammation shifted the voltage-dependence of activation of the tetrodotoxin-resistant current to more hyperpolarized potentials.
  
  
  CONCLUSIONS
  Gastric injury alters the properties of Na+ currents in gastric sensory neurons. This may enhance excitability, thereby contributing to the development of dyspeptic symptoms.
authors.affiliation: Department of Internal Medicine, College of Medicine, The University of Iowa, Iowa City, Iowa 52242, USA. klaus-bielefeldt@uiowa.edu
authors.forename: K
authors.initials: K
authors.lastname: Bielefeldt
authors.forename: N
authors.initials: N
authors.lastname: Ozaki
authors.forename: G F
authors.initials: GF
authors.lastname: Gebhart
mesh_terms: D019342:Acetic Acid; D000779:Anesthetics, Local / Q000494:pharmacology; D000818:Animals; D004195:Disease Models, Animal; D005727:Ganglia, Spinal / Q000166:cytology; D005756:Gastritis / Q000139:chemically induced / Q000503:physiopathology; D006930:Hyperalgesia / Q000503:physiopathology; D015640:Ion Channel Gating / Q000187:drug effects / Q000502:physiology; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009475:Neurons, Afferent / Q000502:physiology*; D009620:Nodose Ganglion / Q000166:cytology; D018408:Patch-Clamp Techniques; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000378:metabolism*; D015222:Sodium Channels / Q000502:physiology*; D013270:Stomach / Q000294:innervation / Q000503:physiopathology; D013276:Stomach Ulcer / Q000139:chemically induced / Q000503:physiopathology*; D013779:Tetrodotoxin / Q000494:pharmacology
chemical_list: D000779:Anesthetics, Local; D015222:Sodium Channels; D013779:Tetrodotoxin; D012964:Sodium; D019342:Acetic Acid