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. 1982 May:326:527-51.
doi: 10.1113/jphysiol.1982.sp014210.

Properties of miniature excitatory junctional currents at the locust nerve-muscle junction

Properties of miniature excitatory junctional currents at the locust nerve-muscle junction

S G Cull-Candy et al. J Physiol. 1982 May.

Abstract

1. Miniature excitatory junctional currents (m.e.j.c.s) were examined in conditions where inward current was carried mainly by Na(+) (i.e. in normal medium, Ca(2+)-free medium and Cl(-)-free medium). M.e.j.c.s were also examined in isotonic Ca(2+) where the inward post-synaptic current was carried mainly by Ca(2+).2. In normal medium, mean m.e.j.c. amplitude = 2.34+/-0.05 nA. The decay time constant of m.e.j.c.s (excluding a small percentage with abnormal shapes) was tau(m.e.j.c.) = 2.62+/-0.11 msec (V(m) = -80 mV, T = 22 degrees C). Decay-time was not markedly changed in Ca(2+)-free or Cl(-)-free medium. tau(m.e.j.c.) approaches the life-time of glutamate activated junctional channels.3. Excitatory junctional currents, evoked by nerve impulses, decayed slightly faster than m.e.j.c.s obtained in the same fibres. Extracellularly recorded m.e.j.c.s and voltage-clamped m.e.j.c.s were similar in time course.4. tau(m.e.j.c.) decreased exponentially with membrane hyperpolarization. An e-fold change was produced by 182.+/-24.8 mV change in V(m).5. The dependence of mean m.e.j.c. amplitude on clamp potential showed a slight non-linearity at hyperpolarized levels. The equilibrium potential for transmitter action was close to 0 mV in normal solution as well as in Ca(2+)-free and Cl(-)-free solutions.6. The kinetics of junctional channels are altered in isotonic Ca(2+). M.e.j.c. amplitude was reduced to about one-third normal size; mean m.e.j.c. = 0.74+/-0.03 nA. The decay time becomes markedly briefer, tau(m.e.j.c.) = 1.01+/-0.08 msec, indicating a reduction in mean channel life-time (V(m) = -80 mV, T = 22 degrees C).7. A population of slow time course and composite m.e.j.c.s appear when muscle fibres are hyperpolarized in isotonic Ca(2+), thus producing a prolongation in mean tau(m.e.j.c.). This results from an influence of post-synaptic membrane potential on presynaptic transmitter release. If such m.e.j.c.s are ignored the voltage dependence of tau(m.e.j.c.) of the remaining events is abolished or even reversed indicating that voltage sensitivity of channel life-time is altered in isotonic Ca(2+). The equilibrium potential for transmitter action may be slightly more positive than normal.8. We estimate that a single packet of neurally released transmitter normally opens, on average, 250 ion channels at these junctions.

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