| Research Abstract |
Interleukin-1 (IL-1) is a cytokine which possesses a wide range of activities in inflammatory, metabolic, haemopoietic and immunological states. Although it is likely that IL-1beta modulates autonomic functions and affect stress processing in various peripheral organs, the effect of IL-1beta on the function of peripheral autonomic neurons is not investigated, in vitro. The aim of the present study was to examine the effect of interleukin-1beta (IL-1beta) on neuronal membrane and synaptic transmission in mammalian pelvic ganglia and bullfrog sympathetic ganglia, in vitro. Bath-application of recombinant human IL-1beta (6 pM-300 nM) for 10 s produced a long-lasting hyperpolarization associated with decreased input resistance in 11 neurons rat major pelvic ganglia (MPG). In other 8 neurons, IL-1beta produced a biphasic response which consists of an initial depolarization followed by a long-lasting hyperpolarization. TTX (3 muM) did not block these responses to IL-1beta. Active fragment of
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IL-1beta (IL-1beta 163-171, 10-100 pM), he active domain of human IL-l(beta, mimicked the effects of IL-1beta. Picrotoxin (100 muM) depressed not only initial depolarization but also hyperpolarization induced by IL-13b (300 nM). These results suggest that yaminobutyric acid (GABA) mediates the biphasic response produced by IL-1beta via GABA_c receptors. Since db-cyclic guanosine monophosphate (GMP) produced an initial depolarization followed by a long-lasting hyperpolarization, cyclic GMP might mediate, at least in part, the IL-1beta-induced hyperpolarization in rat MPG neurons. IL-1beta caused an initial facilitation followed by a long-lasting depression of the EPSP in rabbit vesical pelvic ganglia (VPG) evoked by stimulation of the pelvic nerve. TL-1beta did not affect the depolarizing response produced by acetylcholine (ACh), suggesting that IL-1beta reduces the release of ACh from the pelvic nerve terminals. It is likely that IL-1beta may inhibit the functions of the urinary bladder and other pelvic organs. Less
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