Recombinant human interleukin-1 beta alters the activity of preoptic thermosensitive neurons in vitro.

Effects of recombinant human interleukin-1 beta (rhIL-1 beta) on the single activity of thermosensitive and thermally insensitive neurons in the preoptic and anterior hypothalamus (PO/AH) were investigated in the rat's brain tissue slices. RhIL-1 beta (2.8 X 10(-9)-1.2 X 10(-8) M) decreased the activity in 19 of 27 warm-sensitive neurons and excited 2 of 3 cold-sensitive neurons, but had no effect on the majority (22 of 32) of thermally insensitive neurons. The neuronal responses to local rhIL-1 beta could be observed in a Ca2+ free/high Mg2+ solution, suggesting the postsynaptic actions of rhIL-1 beta. The actions of rhIL-1 beta on thermosensitive neurons were blocked or attenuated by concurrent application of sodium salicylate, but not by naloxone. The results suggest that centrally formed IL-1 beta may induce fever by its actions on PO/AH thermosensitive neurons, which do not involve the opioid receptor mechanisms.