Intracellular recordings were obtained from CA1 neurons of rat hippocampal slices preparation. Dopamine applied by perfusion (10-5-10-7 M), microdrop (10-4M) and iontophoresis (+80, +200 nA balanced current) inhibited "spontaneous" and evoked action potentials. An increase in current injection restored the evoked action potentials which appeared unmodified. Membrane potential was not modified in 60% of the neurons; in the remaining ones, a slow depolarization was observed. Membrane resistance, measured at rest, was not modified by dopamine. Calcium-mediated events such as bursting activity and afterhyperpolarization, mainly in the late component, were also attenuated by the catecholamine. These effects were antagonized by domperidone, a dopaminergic antagonist. Calcium spikes, evoked in tetrodotoxin- and tetraethylammonium-poisoned slices, were reversibly inhibited by dopamine. Since an increase in the amplitude of a depolarizing pulse of injected current was able to evoke both sodium and calcium action potentials suppressed by dopamine without change in shape or duration, it is concluded that this catecholamine depresses cellular excitability by altering the interaction between membrane voltage and sodium and calcium entry and the subsequent increase in potassium conductance.
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