Mild gastritis alters voltage-sensitive sodium currents in gastric sensory neurons in rats.
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.[1]References
- Mild gastritis alters voltage-sensitive sodium currents in gastric sensory neurons in rats. Bielefeldt, K., Ozaki, N., Gebhart, G.F. Gastroenterology (2002) [Pubmed]
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