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1 Department of Pharmacology, The University of Iowa, Iowa city, Iowa, USA
2 Department of Internal Medicine, The University of Iowa, Iowa city, Iowa, USA
* To whom correspondence should be addressed. E-mail: khoa-dang{at}uiowa.edu.
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 (DiI) 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 injections (SAL) 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), while 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.
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