Human recombinant interleukin-1 inhibits nicotinic transmission in
neurons of guinea pig pelvic plexus ganglia.
Lin, Jingyang, and Jacob Krier.
Department of Physiology, Michigan State University, East Lansing,
Michigan 48824
APStracts 2:0129G, 1995.
The actions of human recombinant interleukin-1 (hrIL-1 ) were tested
on guinea-pig pelvic plexus ganglion neurons using intracellular
electrophysiological methods in vitro. HrIL-1 caused membrane
depolarization associated with a decreased input resistance or inward
currents in 54% of neurons tested. HrIL-1 caused a hyperpolarization
associated with an increase in input resistance or outward currents
in 30% of neurons tested. HrIL-1 -evoked responses were not altered
by hexamethonium (100 [mu]M), atropine (0.5 [mu]M), yohimbine (0.3
[mu]M) or naloxone (1 [mu]M) indicating that cholinergic, [alpha]2
-adrenergic or opioid receptors were not involved. Drugs that inhibit
Na-, Ca2- or K- channels, did not change hrIL-1 -evoked responses.
Stimulation of synaptic inputs to pelvic ganglion neurons evoked
nicotinic cholinergic fast excitatory post synaptic potentials (f
-EPSPs). HrIL-1 inhibited f-EPSPs in 44% of neurons tested but had no
effect on acetylcholine-induced depolarizations. An IL-1 receptor
antagonist blocked all actions of hrIL-1 . In summary, hrIL-1 has
excitatory and inhibitory actions on pelvic ganglion neurons.
Inhibition of f-EPSPs by hrIL-1 may be due to presynaptic inhibition
of acetylcholine release.
Received 13 April 1995; accepted in final form 14 June 1995
APS Manuscript Number G0156-5.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 11 July 1995.