Deficits in Endogenous Adenosine Formation by Ecto-5′-Nucleotidase/CD73 Impair Neuromuscular Transmission and Immune Competence in Experimental Autoimmune Myasthenia Gravis

Figure 6

Dephosphorylation of AMP, to ADO via ecto-5′-nucleotidase/CD73, facilitates the release of [³H]-ACh from stimulated phrenic motor nerve terminals of naïve, control, and EAMG rats. (a) and (b) show the kinetics of the extracellular AMP (30 M) catabolism (a) and formation of ADO plus nucleoside derivatives (inosine (INO) and hypoxanthine (HX)) (b) in hemidiaphragm preparations from naïve, control, and EAMG rats. AMP (30 M) was added to the preparation at zero time; samples were collected from the bath at indicated times on the abscissa and retained for HPLC analysis. Data shown are averages pooled from 4 naïve, 6 control, and 6 EAMG animals. The vertical bars represent SEM and are shown when they exceed the symbols in size. (c) Facilitatory effects of AMP (100 M) on evoked [³H]-ACh release (5 Hz, 750 pulses, and ) from hemidiaphragm preparations from naïve, control, and EAMG rats. AMP (100 M) was applied 15 min before . Each column represents pooled data from 4 (naïve and control) and 7 (EAMG) animals. The vertical bars represent mean SEM.

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