[Rapid inhibitory effect of glucocorticoids on ACh-induced current in rat phaeochromocytoma cells].
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 PC12 cells was proved to be generated through nicotinic ACh receptor by pharmacological identification. ACh (30 mumol/L) induced an inward current at a holding potential (Vh) of -80 mV. The inhibitory effect of corticosterone (B) on IACh was weak when 10(-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. Taken together, it is suggested that GC induced rapid inhibitory effects on IACh in PC12 cells are probably mediated by a nongenomic mechanism. The inhibitory effect of various GC on IACh are different.
Shi
L J
LJ
Department of Physiology, Department of Basic Medicine, Second Military Medical University, Shanghai 200433.
Wang
C A
CA
Chen
Y Z
YZ
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D003345:Corticosterone / Q000494:pharmacology; D003907:Dexamethasone / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005938:Glucocorticoids / Q000494:pharmacology*; D006854:Hydrocortisone / Q000494:pharmacology; D008564:Membrane Potentials; D016716:PC12 Cells / Q000502:physiology; D051381:Rats
D005938:Glucocorticoids; D003907:Dexamethasone; D000109:Acetylcholine; D003345:Corticosterone; D006854:Hydrocortisone