Journal
GASTROENTEROLOGY
Volume 122, Issue 2, Pages 394-405Publisher
W B SAUNDERS CO
DOI: 10.1053/gast.2002.31026
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Funding
- NIDDK NIH HHS [DK01548] Funding Source: Medline
- NINDS NIH HHS [NS 35790] Funding Source: Medline
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Background & Aims: 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-tetramethyl-indocarbocyanine 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.
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