Journal
GASTROENTEROLOGY
Volume 122, Issue 3, Pages 752-761Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1053/gast.2002.31901
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Funding
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS035790] Funding Source: NIH RePORTER
- NIDDK NIH HHS [DK01548] Funding Source: Medline
- NINDS NIH HHS [NS 35790] Funding Source: Medline
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Background & Aims: Visceral hypersensitivity can be found in more than one third of patients with dyspeptic symptoms. We hypothesized that peripheral sensitization plays an important role in the development of hypersensitivity. Methods: We induced mild gastritis in Sprague-Dawley rats by adding 0.1% iodoacetamide to the drinking water. The stomach was injected with a retrograde label to identify gastric sensory neurons. Nodose and T9, T10 dorsal root ganglia were removed 7 days after initiation of iodoacetamide treatment. The cells were dissociated and cultured for 3-8 hours before recording whole cell currents using the patch-clamp technique. Results: Iodoacetamide induced a mild gastritis. Although there were no changes in voltage-sensitive inward and outward currents in nodose neurons, the inward currents increased significantly in T9, T10 spinal neurons. A more detailed analysis of sodium currents showed that this was caused by an increase in the tetrodotoxin-resistant sodium current. Conclusions: Mild gastritis increases the tetrodotoxin-resistant current in gastric spinal sensory neurons. Considering the importance of sodium currents as determinants of neuron excitability, this change may contribute to peripheral sensitization and enhanced neuron excitability.
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