DIHYDROPYRIDINE-SENSITIVE CA2+ SPIKES AND CA2+ CURRENTS IN RABBIT CILIARY BODY EPITHELIAL COILS

Intracellular microelectrode and whole-cell patch-clamp recordings were used to investigate a Ba2+-induced regenerative depolarization and its underlying Ba2+ current in the ciliary body epithelial cells of the rabbit eye. Exposure of these epithelial cells to 4-10 mmol l-1 Ba2+ depolarized the membrane potential and caused the generation of one or more spikes, before the membrane potential reached a steady-state level. The spikes, but not the slow phase of depolarization, could be blocked with Co2+ (2 mmol l-1), Gd3+ (25 μmol l-1), La3+ (20 μmol l-1), Cd2+ (10 μmol l-1), verapamil (30 μmol l-1) and nifedipine (1 μmol l-1). Tetrodotoxin at 100 nmol l-1 had no effect. In the absence of Na+, but in the presence of external Ba2+, step depolarization of the membrane potential activated an inward current that could be blocked with Co2+ (2 mmol l-1), Cd2+ (10 μmol l-1) and nifedipine (1 μmol l-1), but not with Ni2+ (50 μmol l-1) or ω-conotoxin (1-10 μmol). This inward current could be enhanced with the dihydropyridine agonist (±)BAY K 8644 (1 μmol l-1). The inactivation characteristics of the inward current (v(1/2) = -38.7 mV, k = 12.6 mV) is most like that seen in neurons. These findings indicate that the epithelial cells of the ciliary body possess dihydropyridine-sensitive, voltage-activated Ca2+ channels. © 1994 Academic Press. All rights reserved.