Functional aspects of dexamethasone upregulated nicotinic acetylcholine receptors in C2C12 myotubes.

Three days of treatment with the glucocorticoid dexamethasone (1 nM-1 microM) induced a concentration-dependent up-regulation of muscle nicotinic acetylcholine receptor (nAChR) in C2C12 mouse myotubes (EC50 = 10 +/- 7.3 nM), as assessed by [3H]alpha-BuTx binding. The maximum increase in binding amounted 148 +/- 17.6% of control. Parallel electrophysiological measurements employed the patch-clamp technique in cell-attached configuration. The nAChR single channel properties were investigated in the presence of carbachol (1 microM) in the pipette. Treatment with dexamethasone (1 microM, 1-5 days) induced an increase in the number of patches showing channel activity from 30 to 70%. Ion channel characteristics did not differ significantly in control and dexamethasone treated myotubes. Conductance was 32 +/- 3 vs 31 +/- 2 pS, respectively. The time constants of open time events tau 1 and tau 2 were 0.6 +/- 0.1 and 6.6 +/- 1 ms vs 0.6 +/- 0.1 and 6.6 +/- 1 ms, respectively. Closed duration's tau 1 and tau 2 were 1.1 +/- 0.2 and 110 +/- 12 ms vs 1.2 +/- 0.3 and 107 +/- 18 ms. In conclusion, dexamethasone upregulated nAChRs are functional and their electrophysiological parameters are similar to those found in control myotubes.