Abstract
In the present study the relationship between tissue damage and changed electro-physiological properties of Dogiel type II myenteric neurons within the first 24 hours after induction of inflammation with trinitrobenzene sulfonate (TNBS) in the guinea-pig ileum was investigated. Treatment with TNBS causes damage to the mucosa, inflammatory responses in the mucosa and enteric ganglia and changes in myenteric neuron properties. Thus we hypothesise that the physiological changes in the myenteric neurons could be due to damage to their mucosal processes or inflammation in the vicinity of cell bodies or the processes. We found an association between hyperexcitability of myenteric Dogiel type II neurons and damage to the mucosa and its innervation at 3 and 24 h, times when there was also an inflammatory reaction. The lack of hyperexcitability in neurons from control tissues in which axons projecting to the mucosa were severed suggests that inflammation may be an important contributing factor to the neuronal hyperexcitability at the acute stage of inflammation. Despite mucosal repair and re-innervation of the mucosa before 7 days after induction of inflammation, neuronal hyperexcitability persists. Although the mechanisms underlying neuronal hyperexcitability at the acute stage of inflammation might be different from those underlying long-term changes in the absence of active inflammation in the ganglia, the persistent changes in neuronal excitability may contribute to post-inflammatory gut dysfunctions.