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INFLAMMATION/IMMUNITY/MEDIATORS
Departments of 1Pharmacology and 2Internal Medicine, The University of Iowa, Iowa City, Iowa 52242
Submitted 12 June 2003 ; accepted in final form 1 October 2003
Voltage-dependent potassium currents are important contributors to neuron excitability and thus also to hypersensitivity after tissue insult. We hypothesized that gastric ulcers would alter K+ current properties in primary sensory neurons. The rat stomach was surgically exposed, and a retrograde tracer (1,1'-dioctadecyl-3,3,3,3'-tetramethylindocarbocyanine methanesulfonate) was injected into multiple sites in the stomach wall. Inflammation and ulcers were produced by 10 injections of 20% acetic acid (HAc) in the gastric wall. Saline (Sal) injections served as control. Nodose or T9–10 dorsal root ganglia (DRG) cells were harvested and cultured 7 days later to record whole cell K+ currents. Gastric sensory neurons expressed transient and sustained outward currents. Gastric inflammation significantly decreased the A-type K+ current density in DRG and nodose neurons (Sal vs. HAc-DRG: 82.9 ± 7.9 vs. 46.5 ± 6.1 pA/pF; nodose: 149.2 ± 10.9 vs. 71.4 ± 11.8 pA/pF), whereas the sustained current was not altered. In addition, there was a significant shift in the steady-state inactivation to more hyperpolarized potentials in nodose neurons (Sal vs. HAc: -76.3 ± 1.0 vs. -83.6 ± 2.2 mV) associated with an acceleration of inactivation kinetics. These data suggest that a reduction in K+ currents contributes, in part, to increased neuron excitability that may lead to development of dyspeptic symptoms.
stomach; visceral inflammation; hyperalgesia; dorsal root ganglia; nodose ganglia; voltage clamp; 4-aminopyridine; dendrotoxin; K+ currents
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