SUMMARY1. End-plate potentials were recorded intracellularly at the frog neuromuscular junction bathed in a solution containing a low concentration of calcium and a high concentration of magnesium.2. The muscle was subsequently subjected to 'cholinesterase staining', and the area of the individual end-plates, studied with intracellular electrodes, was measured.3. A positive correlation was found between the end-plate area and the diameter of muscle fibres.4. The mean quantum content (m) showed a positive correlation with the size of end-plates.5. The frequency of spontaneous miniature end-plate potentials was positively correlated with m as well as with end-plate area.6. It is concluded that the amount of transmitter released following nerve stimulation is related to the size of nerve endings.

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SUMMARY1. Monosynaptic excitatory post-synaptic potentials (EPSPs) produced in triceps surae motoneurones of the cat by stimulation of single afferent fibres in the muscle nerve were recorded with intracellular electrodes before and after the administration of thiopentone or pentobarbitone.2. The average amplitude of the 'unit' EPSP was 0-11-0-21 mV and remained unchanged after the administration of the barbiturates (10 mg/ kg, I.V.).3. Mean quantum content (m) ranged from 1-9 to more than 5 before drug administration. The m was reduced by thiopentone (10 mg/kg, i.v.) and pentobarbitone (10 mg/kg, i.v.) by 23-1 and 24-7 % respectively. 4. The barbiturates, in the doses employed, produced no alterations in the input resistance of the motoneurone membrane or in the strengthduration relation obtained by passing depolarizing current pulses through the micro-electrode.5. It is concluded that the action of thiopentone and pentobarbitone, in the doses used, is confined to the presynaptic nerve terminals and results in a reduction in the amount of transmitter released by afferent impulses.

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SUMMARY1. Cobalt ions, in concentrations of 0-05-2 mm, block neuromuscular transmission in the frog sartorius muscle.2. The reduction in the e.p.p. amplitude produced by Co2+ is due to a decrease in the amount of transmitter released by a nerve impulse (mean quantum content). This reduction is associated with little change in the resting membrane potential of the muscle fibre or in the mean amplitude of spontaneous m.e.p.p.s.3. The reduction in evoked transmitter release produced by Co2+ may be antagonized by elevation of the external Ca2+ concentration. It is suggested that the antagonism between Co2+ and Ca2+ is competitive in nature.4. The mean dissociation constant for Co2+ and its hypothetical membrane complex was found to be 0418 mm. On this basis, it is concluded that Co2+ is about 20 times more potent than Mg2+ in suppressing evoked transmitter release.5. In contrast to the inhibitory action on evoked release, Co2+ increases spontaneous transmitter release. However, concentrations of Co2+ 20-60 times greater than those which decrease the e.p.p. amplitude are needed to produce a significant increase in m.e.p.p. frequency.