Inhibition of the calcitonin-induced outward current in identified Aplysia neurons by interleukin-1 and interleukin-2.

1. The effects of bath-applied recombinant human interleukin-1 (rhIL-1) and interleukin-2 (rhIL-2) on the calcitonin (CT)-induced outward current recorded from identified neurons (R9-R12) of Aplysia kurodai were investigated with conventional voltage-clamp and pressure ejection techniques. 2. Micropressure ejection of CT onto the soma of the neuron induced a slow outward current [Io(CT); 4-6 nA in amplitude, 30-40 sec in duration] associated with a decrease in input membrane conductance. 3. Io(CT) was increased by hyperpolarization. 4. The extrapolated reversal potential was +10 mV. Additionally, Io(CT) was sensitive to changes in (Na+)o but not to changes in (K+)o, (Ca2+)o, and (Cl-)o. 5. Micropressure-ejected forskolin produced a slow outward current similar to that induced by CT. 6. Bath-applied rhIL-1 and rhIL-2 (10-40 U/ml) reduced the CT-induced current in identified Aplysia neurons without affecting the resting membrane conductance or the holding current. 7. The inhibitory effects of both cytokines on the current were completely reversible. Heat-inactivated rhIL-1 and rhIL-2 were without effect. 8. These results suggest that the immunomodulators, IL-1 and IL-2, can modulate the CT-induced outward current associated with a decrease in Na+ conductance in the nervous system of Aplysia. Therefore, the study suggests that these cytokines may also serve as neuromodulators.