Abstract
The effect of central administration of interleukin-1β on naloxone-precipitated withdrawal in morphine-dependent mice was studied. The degree of physical dependence on morphine was estimated by counting the number of jumps precipitated by naloxone, one of the typical withdrawal signs. Intracisternal (i.c.) administration of interleukin-1β (0.01 – 1 ng/5 μl per mouse) to morphine-dependent mice 30 min prior to the injection of naloxone (10 mg/kg i.p.) decreased the number of jumps in a dose-dependent manner. The effect of interleukin-1β (1 ng) was significantly antagonized when it was co-administered with interleukin-1 receptor antagonist (1 μg/mouse). These results suggest that centrally administered interleukin-1β could attenuate naloxone-precipitated withdrawal in morphine-dependent mice via interleukin-1 receptors in the brain. Co-administration of α-melanocyte-stimulating hormone (300 ng/mouse) or α-helical corticotropin-releasing factor (CRF)-(9–41), a CRF receptor antagonist (300 ng/mouse), with interleukin-1β also antagonized the inhibitory effect of interleukin-1β (1 ng). Moreover, i.c. administration of CRF (200 ng/mouse) significantly decreased the number of jumps.
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