Feed-Forward Inhibition of CD73 and Upregulation of Adenosine Deaminase Contribute to the Loss of Adenosine Neuromodulation in Postinflammatory Ileitis
Figure 2
(a) Actions of selective adenosine A1 and receptor antagonists on [3H]-ACh release from myenteric motoneurons stimulated electrically (5 Hz, 200 pulses, 1 ms duration). DPCPX (10 nM, A1 receptor antagonist) and ZM 241385 (50 nM, receptor antagonist) were added to the incubation media before the second period of stimulation (S 2) and were present throughout the assay. The ordinates are changes in S 2/S 1 ratios compared to the S 2/S 1 ratio obtained in control conditions, that is, with no drugs added. The data are means ± SEM of three to five individual experiments. (one-way ANOVA followed by Dunnett’s modified t-test) represent significant differences when compared to the situation where no drugs were added (dashed line). (b) Confocal images of whole-mount preparations of longitudinal muscle-myenteric plexus preparations of the ileum from control and TNBS-injected rats. Adenosine A1 receptor immunoreactivity is predominantly present in ganglion neuronal cell bodies in control and TNBS-injected preparations. Adenosine receptor imunoreactivity is mainly present in nerve bundles and axon terminals of myenteric neurons (triangles). In inflamed preparations, adenosine receptor staining is also observed in few mononuclear cells infiltrating the neuromuscular layer (arrows).
