The effect of voltage on the time course of end‐plate currents

Abstract

SUMMARY1. End-plate currents have been studied in glycerol-treated frog sartorius nerve-muscle preparations with the voltage clamp technique.2. End-plate currents follow a simple exponential time course over most of their declining phase.3. The rate constant ac that characterizes this exponential decay depends upon membrane potential V according to the relationship a (V) = BeAV, with A = 0-00795 + 000043 (s.E.) mV-1 and B = 1-67 + 0 04 (S.E.) msec-1.4. Voltage sensitivity decreases (that is, A in the above equation becomes smaller) as the recording and current-passing electrodes are moved away from the end-plate region.5. The voltage sensitivity of ax is decreased by decreasing the gain of the voltage clamp amplifier.6. Changing the end-plate current amplitude by curare treatment, by increased calcium ion concentration, and by facilitation and depression has essentially no effect on end-plate current time course.7. When membrane potential is changed step-wise during the decaying phase of the end-plate conductance change, currents begin to decline with a rate constant ax appropriate to the new membrane potential in less than 0-2 msec.8. Treatment with prostigmine methylsulphate in concentrations up to 50 ,ug/ml. slows end-plate current decay but has little effect on voltage sensitivity. That is, B in the above equation is decreased by prostigmine treatment, but A is relatively unaffected.

Analysis of current noise evoked by nicotinic agonists in rat submandibular ganglion neurones

“…in the presence of 25 JAM CCh to that in the presence of 5OjAM CCh was 1.03±15% (ratio of the means ± coefficient of variance), the mean ratio for ACh, CCh and DMPP at -60 mV and -80 mV was 1.06± 13%. (Rang, 1981) and of the endplate currents in frog muscle (Magleby & Stevens, 1972 for the difference in potential step. The relative contribution of the fast component to the total varnents in the spectra are supposed to originate from iance, expressed as far, appeared to be rather greater two independent channel populations, T1 and T2 can at -40 mV than at -80 mV, the ratio be interpreted as 1/al and 1/a2 (the mean channel fa,rl(-40mV)/far(-80mV) being 1.8±0.32 (6 lifetimes) respectively, provided that pi(oo) is close to cells).…”

The Action of Polymyxin B at the Frog Neuromuscular Junction

“…Such an action is explained by the accumulation of calcium in the nerve terminal which overcomes the magnesium-induced (Lee et al, 1977;Singh et al, 1978). In vivo, 4-aminopyridine has been shown to reverse polymyxin B-induced block of the indirectly stimulated tibialis anterior muscle of the cat (Lee, de Silva & Katz, 1978 (Magleby & Stevens, 1972). Recently the antibiotics, lincomycin and clindamycin, have been shown to alter miniature e.p.c.…”

“…tetraethylammonium (Alder, Oliveira, Albuquerque, Mansour & Eldefrawi, 1979) and lobeline (Lambert, Reynolds, Volle & Henderson, 1979). The Tls of e.p.cs recorded from endplates treated with glycerol (Magleby & Stevens, 1972), low concentrations of (+}tubocurarine (Katz & Miledi, 1978) or alpha bungartoxin (Katz & Miledi, 1978) and the T4 of untreated m.e.p.cs (Gage & McBurney, 1975) have been shown to vary with holding potential, becoming longer at more hyperpolarized potentials.…”

Equilibrium Potential for the Postsynaptic Response in the Squid Giant Synapse

“…Kordas suggested that acetylcholine caused an increase in the Na+ and K+ conductance via a single channel which had a voltage-sensitive time-course. This voltage sensitivity of the EPC has been studied extensively by Magleby and Stevens (1972) and the proposed voltage dependence has been used to formulate a theory of the action of acetylcholine that involves the dipole moment of the acetylcholine-receptor complex. The magnitude of the change in time constant for decay of the EPC is from 1.6 ms at a potential of -100 mV to 0.4 ms at a potential of +90 mV.…”