Abstract
A rapid effect of glucocorticoids (GC) on acetycholine-induced current in rat phaeochromocytoma (PC12) cells and its possible mechanism were investigated by whole-cell clamp technique. The results are as follows: The acetylcholine-induced current (IACh) of PCl2 cells was proved to be generated through nicotinic ACh receptor by pharmacological identification. ACh (30 μmol/L) induced an inward current at a holding potential (Vh)of-8O mV. The inhibitory effect of corticosterone (B) on IACh was weak when 140-5 mol/L B and ACh were simultaneously applied extracellularly. Pretreatment of PC12 cells with B could augment the inhibitory effect on peak IACh, and this dose-dependent effect was reversible. At the same concentration of GC, the rank of the inhibitory potency was B > dexamethasone (Dex) > hydrocortisone (F). Extracellular application of B-BSA could also inhibit IACh rapidly.
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Citing This Article：
, , . . Acta Physiol Sin 1998; 50 (6): (in Chinese with English abstract).
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