Effects of recombinant human interleukin-1 beta (IL-1 beta) on the neuronal activities in the rat dorsal motor nucleus of the vagus (DMV) were investigated by extra- and intracellular recordings in slice preparations. Twelve (52%) of 23 spontaneously firing neurons recorded extracellularly, 7 of which were electrophysiologically identified as vagal motoneurons, were inhibited by a bath application of IL-1 beta at a dose of either 5.8 x 10(-8) or 5.8 x 10(-8) M. The duration of the responses ranged widely from about 10 min to more than 2 h. Two (9%) of the 23 neurons were excited, whereas the remaining 9 (39%) were not affected by IL-1 beta. Of 42 DMV neurons recorded intracellularly, 19 (45%) showed a hyperpolarization following an application of 5.8 x 10(-8) M IL-1 beta, which still persisted in a TTX-containing solution. Two (5%) displayed depolarization and 21 (50%) were unaffected. The hyperpolarization in 16 of the 19 neurons (84%) ranged from -5 to -10 mV and lasted for more than 30 min without changing the input resistance. The IL-1 beta-induced hyperpolarization was completely blocked by concurrent perfusion with sodium salicylate. The remaining three neurons showed a short-lasting (5-14 min) hyperpolarization (ranging from -6 to -15 mV) with a decrease in the input resistance. These findings indicate that IL-1 beta mainly inhibits the vagal motoneurons in the DMV, at least partly through prostaglandin synthesis. This provides a mechanism that could account for the central action of IL-1 beta on visceral processes such as the inhibition of gastric acid secretion.