The effects of vasopressin (VP) on lateral horn cells including a number of sympathetic preganglionic neurons contained in thin in vitro slices of neonatal rat spinal cord were investigated by means of intracellular recording techniques. Superfusion of (Arg8)-vasopressin (AVP, 0.01-1 microM) caused a depolarization leading, in the majority of lateral horn cells, to repetitive discharges. The AVP depolarization which could be partially reduced by low Ca/high Mg solution or tetrodotoxin, was accompanied by an increase in membrane resistance and the response was nullified near the membrane potential at which the spike afterhyperpolarization was abolished. A clear reversal of the response was not observed upon further hyperpolarization. The AVP response was blocked by the VP1 antagonist, D-(CH2)5 Tyr (Me)-AVP, whereas, deamino (D-Arg8-vasopressin), a VP2 agonist, at high concentrations (greater than or equal to 50 microM) was either ineffective or produced a small depolarization. The results indicate that AVP, acting mainly on VP1 receptors, excited lateral horn cells by a direct depolarization and an indirect effect via the release of an excitatory transmitter(s). A reduction of a voltage-dependent K conductance may underlie the depolarizing effect of AVP.