HUMAN RECOMBINANT INTERLEUKIN-1-BETA INHIBITS NICOTINIC TRANSMISSION IN NEURONS OF GUINEA-PIG PELVIC PLEXUS GANGLIA

The actions of human recombinant interleukin-1 beta (hrIL-1 beta) were tested on guinea pig pelvic plexus ganglion neurons using intracellul ar electrophysiological methods in vitro. hrIL-1 beta caused membrane depolarization associated with a decreased input resistance or inward currents in 54% of neurons tested. hrIL-1 beta caused a hyperpolarizat ion associated with an increase in input resistance or outward current s in 30% of neurons tested. hrIL-1 beta-evoked responses were not alte red by hexamethonium (100 mu M), atropine (0.5 mu M), yohimbine (0.3 m u M), or naloxone (1 mu M), indicating that cholinergic, alpha(2)-adre nergic, or opioid receptors were not involved. Drugs that inhibit Na+, Ca2+, or K+ channels did not change hrIL-1 beta-evoked responses. Sti mulation of synaptic inputs to pelvic ganglion neurons evoked nicotini c cholinergic fast excitatory postsynaptic potentials (fEPSPs). hrIL-1 beta-inhibited fEPSPs in 44% of neurons tested but had no effect on a cetylcholine-induced depolarizations. An IL-1 beta receptor antagonist blocked all actions of hrIL-1 beta. In summary, hrIL-1 beta has excit atory and inhibitory actions on pelvic ganglion neurons. Inhibition of fEPSPs by hrIL-1 beta may be due to presynaptic inhibition of acetylc holine release.