Abstract
The role of the proinflammatory cytokines interleukin-lα (IL-lα), interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNFα) in THC-induced catalepsy in mice was examined. Recombinant IL-1β (400 ng/mouse, IV) and TNFα (500 ng/mouse, IV) were effective in potentiating the cataleptic effect of low-dose THC (10 μg/mouse, IV). Recombinant IL-1α and IL-6 did not potentiate catalepsy at any dose tested. Anti-IL-1β and anti-TNFα antibodies were effective in attenuating high-dose (75 μg/ mouse) THC-induced catalepsy. Antibodies to IL-1α and IL-6 had no effect on catalepsy. Early onset catalepsy (10 min postinjection) was potentiated by exogenous recombinant IL-1β and TNFα but only later catalepsy (2 h postinjection) was attenuated by antibodies to endogenous IL-1β or TNFα. This divergence of the cytokine effect suggests that these substances regulate, by different mechanisms, the early and late THC-induced cataleptic response.
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