Previous analysis of single-channel current records has shown that both the opening and closing transitions of chemically activated ion channels are operated by fast and slow kinetic processes. The fast component in the kinetics of channel opening has been interpreted as the reopening of a channel that has just closed. The fast component in the kinetics of channel closure has many possible explanations and is therefore more difficult to interpret. We can gain insight into the closing process by asking whether the lifetimes of successive openings of an acetylcholine receptor channel are correlated in open-state lifetime. Five kinetic models of channel closure are considered. Two of these models predict uncorrelated open-state lifetimes, one predicts correlated open-state lifetimes, and for two others a range of behavior is possible. Acetylcholine receptor channel data from cultured rat muscle are analyzed to show that open-state lifetimes are correlated, eliminating two models of channel gating.

Single Ca2+-dependent K+-channel currents were recorded in intact and excised inside-out membrane patches of the anterior pituitary clone AtT-20/D16-16. The frequency of channel openings and lifetimes depends both on membrane potential and on the Ca2+ concentrations at the inner membrane surface. The curve of the open-state probability of the channel as a function of membrane potential appears to translate along the voltage axis with changes in internal Ca2+ concentration. For Ca2+ concentrations between 10(-7) and 10(-6) M, the shift is consistent with the hypothesis that three Ca2+ ions are required to open a Ca2+-dependent K+ channel. Single channel conductances are estimated to be 124 pS in patches with normal external K+ (5.4 mM) and 208 pS in excised patches with symmetrical K+ (145 mM) across the membrane. Tetraethylammonium (20 mM) added to the cytoplasmic surface reversibly blocks the Ca2+-dependent K+ channel.

Single cholinergic receptor channel currents activated by curare were recorded in tissue-cultured embryonic rat muscle, directly confirming curare's action as a weak cholinergic agonist. In embryonic muscle, curare, in addition to its classical action as a competitive cholinergic antagonist, produces small sustained depolarizations which can be blocked by alpha-bungarotoxin. The single-channel events are of short duration but otherwise exhibit the major features observed with other cholinergic agonists. The single-channel events are blocked by alpha-bungarotoxin. Two values of unit conductance, 30.4 +/- 3.5 pS and 47 +/- 6 pS, were measured in cells from different cultures. Histograms of open-state duration are well fit by a distribution which is a sum of two exponentials, with time constants of 0.33 +/- 0.08 msec for the fast component and 1.84 +/- 0.43 msec for the slow component.

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