Effects of lithium ions on electrical activity in sympathetic ganglia of the bullfrog.
1 The mode of action of lithium on electrical activity in the sympathetic ganglia of the bullfrog has been studied by recording extracellular and intracellular potential changes. Changes in nerve conduction and various types of synaptic transmission were studied when sodium ions in the external solution were totally replaced by equimolar concentrations of lithium ions and also when lithium ions were added to the external Ringer solution.2 Nerve conduction and nicotinic transmission in sympathetic ganglia were completely blocked in sodium-free sucrose solution, but were restored when the preparations were transferred to a sodium-free lithium solution.3 In the sodium-free lithium solution, the slow excitatory postsynaptic potential (e.p.s.p.) and muscarinic acetylcholine-depolarization were restored while the slow inhibitory postsynaptic potential (i.p.s.p.) and the muscarinic acetylcholine-hyperpolarization were not restored. Furthermore, the early after-discharges were accelerated and the inhibition of after-discharges was eliminated. These results support the hypothetical concept that the slow i.p.s.p. is generated by an activation of the electrogenic sodium pump.4 In the sodium-free lithium solution, restoration of nerve conduction and synaptic transmission were transient phenomena; both conduction and transmission were gradually blocked when preparations were soaked in the solution for long periods. The blockade appeared to be due to membrane depolarization.5 When lithium ions (20 mM) were added to the Ringer solution, nicotinic transmission was depressed. The slow e.p.s.p. was also depressed, but less so than the slow i.p.s.p. The early after-discharge was, however, accelerated; presumably due to the marked depression of the slow i.p.s.p. in this solution.6 Changes in synaptic transmission in Ringer solution containing lithium ions could be explained by membrane depolarization, a reduction of acetylcholine release and a depression of the electrogenic sodium pump.7 All results obtained in the present experiments could be explained by supposing that lithium ions are able to substitute for sodium ions in passive ionic membrane transport dependent on electrochemical energy but not in active ionic membrane transport dependent on metabolic energy.
D000200:Action Potentials / Q000187:drug effects*; D000818:Animals; D001001:Anura; D001693:Biological Transport, Active; D004558:Electric Stimulation; D005725:Ganglia, Autonomic / Q000187:drug effects*; D005730:Ganglionic Blockers; D005731:Ganglionic Stimulants; D066298:In Vitro Techniques; D008094:Lithium / Q000494:pharmacology*; D008564:Membrane Potentials / Q000187:drug effects; D009431:Neural Conduction / Q000187:drug effects; D010277:Parasympathomimetics; D011892:Rana catesbeiana; D012964:Sodium / Q000494:pharmacology; D009435:Synaptic Transmission / Q000187:drug effects; D014403:Tubocurarine / Q000494:pharmacology
D005730:Ganglionic Blockers; D005731:Ganglionic Stimulants; D010277:Parasympathomimetics; D008094:Lithium; D012964:Sodium; D014403:Tubocurarine