AJP - Gastrointestinal and Liver Physiology, Vol 269, Issue 6 981-G987, Copyright © 1995 by American Physiological Society
Human recombinant interleukin-1 beta inhibits nicotinic transmission in neurons of guinea pig pelvic plexus ganglia
J. Lin and J. Krier
Department of Physiology, Michigan State University, East Lansing 48824, USA.
The actions of human recombinant interleukin-1 beta (hrIL-1 beta) were
tested on guinea pig pelvic plexus ganglion neurons using intracellular
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 hyperpolarization
associated with an increase in input resistance or outward currents in 30%
of neurons tested. hrIL-1 beta-evoked responses were not altered by
hexamethonium (100 microM), atropine (0.5 microM), yohimbine (0.3 microM),
or naloxone (1 microM), 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 beta-evoked responses. Stimulation of
synaptic inputs to pelvic ganglion neurons evoked nicotinic cholinergic
fast excitatory postsynaptic potentials (fEPSPs). hrIL-1 beta inhibited
fEPSPs in 44% of neurons tested but had no effect on acetylcholine-induced
depolarizations. An IL-1 beta receptor antagonist blocked all actions of
hrIL-1 beta. In summary, hrIL-1 beta has excitatory and inhibitory actions
on pelvic ganglion neurons. Inhibition of fEPSPs by hrIL-1 beta may be due
to presynaptic inhibition of acetylcholine release.
