Abstract
A study was made of the effects of Sr2+ and Ba2+ at synapses in isolated superior cervical ganglia of guinea-pigs. Intracellular recordings of membrane potential were made from ganglion cells in the presence of different concentrations of Ca2+, Sr2+ and Ba2+. The addition of Sr2+ (2-5 mM) caused little change in resting membrane potential; in contrast, Ba2+ (1-6 mM) depolarized the cells and prolonged duration of action potentials. The resting frequency of spontaneous miniature excitatory post-synaptic potentials (min. e.p.s.p.s) was briefly accelerated by addition of either Sr2+ or Ba2+ but subsequently returned to about control levels. Following replacement of Ca2+ by Sr2+, e.p.s.p.s could be evoked during repetitive stimulation of preganglionic axons at a fixed latency after the nerve impulses (phasic transmitter release). Replacement of Ca2+ by Ba2+ produced many asynchronous e.p.s.p.s during trains of impulses (residual transmitter release). By analysis of interaction between Sr2+ and Ca2+, Sr2+ had a partial agonist action on phasic transmitter release. The same analysis applied to Ba2+ failed to demonstrate either a partial agonist or an antagonist action. Both Sr2+ and Ba2+ prolonged e.p.s.p.s. Changes in Sr2+ could mainly be attributed to its effect on cell input resistance; Ba2+ may also prolong the time course of transmitter release. The increased frequency of min. e.p.s.p.s which occurred during repetitive stimulation was potentiated by both Sr2+ and Ba2+, Ba2+ being about twice as potent as Sr2+. This activation of residual transmitter release was independent of action of these ions on phasic release. The reported maintenance by Ba2+ of acetylcholine output from perfused ganglia results from asynchronous release of large numbers of quanta during trains of impulses.