Lithium reduced synaptic transmission and increased neuronal excitability without altering endogenous serotonin, norepinephrine and dopamine in rat hippocampal slices in vitro.

1. Extracellular field potentials were recorded in the CA1 pyramidal cell layer following stimulation of stratum radiatum in rat hippocampal slices during superfusion with different concentrations (1, 2, 5, 10, 20, and 30 mM) of lithium (Li+). Control slices were exposed similarly to choline (Ch+) or sodium (Na+). 2. At high concentrations (greater than or equal to 10 mM), Li+, Ch+ and Na+ reduced the amplitude of the field excitatory postsynaptic potential (EPSP). However, Li+ increased, whereas Ch+ and Na+ reduced the population spike amplitude. Thus, Li+ specifically enhanced the excitability of CA1 pyramidal cells. 3. Electrophysiologically monitored slices, plus an additional group exposed to Li+, Ch+ or Na+ without concomitant field potential recordings, were processed for measurement of endogenous levels of serotonin (5-HT), norepinephrine (NE) and dopamine (DA). The mean endogenous levels of 5-HT and NE were not significantly different in 1-30 mM Li+, Ch+ and Na+. Dopamine contents were unchanged after exposure to Li+ and Na+, but were reduced by Ch+. 4. The non-specific effects of Li+ on synaptic transmission and its specific effects on neuronal excitability appeared independent of changes in endogenous 5-HT, NE and DA levels.