Functional aspects of dexamethasone upregulated nicotinic acetylcholine receptors in C2C12 myotubes

Three days of treatment with the glucocorticoid dexamethasone (1 nM-mu M) induced a concentration-dependent up-regulation of muscle nicotinic acetylcholine receptor (nAChR) in C2C12 mouse myotubes (EC(50)=10+/-7.3 nM), as assessed by [H-3]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 mu M) in the pipette. Treatment with dexamethasone (1 mu 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 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. (C) 1995 The Italian Pharmacological Society