Functional aspects of dexamethasone upregulated nicotinic acetylcholine receptors in C2C12 myotubes

Three days of treatment with the glucocorticoid dexamethasone (1 nm-1 ?m) induced a concentration-dependent up-regulation of muscle nicotinic acetylcholine receptor (nAChR) in C2C12 mouse myotubes (EC=10±7.3 nm), as assessed by [H]?-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 ?m) in the pipette. Treatment with dexamethasone (1 ?m, 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 ?1 and ?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 ?1 and ?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. © 1995 The Italian Pharmacological Society.