Reduction of cerebellar GABAA responses by interleukin-1 (IL-1) through an indomethacin insensitive mechanism.

Recently, a role of IL-1 in the central nervous system has been described, principally a fever-inducing effect in the hypothalamus through a prostaglandin second messenger system. IL-1 has also been shown to potentiate gamma-aminobutyric acid (GABAA) responses in embryonic chick neurones. This study describes the investigation of the effect of IL-1 on GABAA responses within the in vitro rat cerebellar slice, a preparation containing intact neuronal circuitry. Stimulation of the area of passage of paralleled fibres produced a pure GABAA inhibition of the spontaneous firing of Purkinje cells. 5 and 10 ng/ml IL-1 produced a reduction in the duration of inhibition 10 min after beginning perfusion of IL-1. This effect reversed within 15 min of washing out the IL-1. 10 ng/ml IL-1 also reduced the effects of exogenously-applied GABA (0.1 mM) with the same time course. In the presence of 1 uM indomethacin, there was no change in the effect of the IL-1. It can therefore be concluded that the reduction in cerebellar GABAA responses by IL-1 is not mediated by the indomethacin-sensitive prostaglandin second messenger system.