Table 2.
No mice with seizures
|
Onset,
min
|
Duration, min
|
||||
---|---|---|---|---|---|---|
Clonic | Tonic | Clonus | Tonus | Clonus | Tonus | |
Wild type | 15/15 | 15/15 | 2.6 ± 0.2 | 5.8 ± 0.6 | 118.2 ± 7.3 | 4.3 ± 0.7 |
Wild type + IL-1Ra | 15/15 | 15/15 | 5.6 ± 0.5* | 12.1 ± 1.3* | 102.4 ± 6.8 | 1.1 ± 0.1* |
Knockout | 10/10 | 10/10 | 3.3 ± 0.3† | 7.5 ± 0.6* | 108.0 ± 10.4 | 2.7 ± 0.3 |
Knockout + IL-1Ra | 10/10 | 9/10 | 3.7 ± 0.8† | 7.4 ± 0.7* | 134.0 ± 11.0 | 3.3 ± 0.5 |
Data are the mean ± S.E.M. Fractions represent the number of 129/SV PasIco mice showing clonic or tonic seizures on the total number of mice. Bicuculline methiodide was injected at a dose of 0.97 nmol in 0.5 μl unilaterally in the dorsal hippocampus. IL-1Ra (0.3 nmol in 0.5 μl) was injected at the same site as bicuculline, 5 min before the convulsant. Recombinant IL-1Ra significantly delayed the onset of clonic and tonic seizures and reduced the duration of tonic convulsions in wild-type littermate mice, whereas it was ineffective in IL-1R type I-deficient mice. Note the delayed onset of clonic and tonic seizures in IL-1R type I-deficient mice (knockout) compared to wild-type littermate mice. Wild-type and knockout mice were injected with heat-inactivated cytokine before bicuculline.
, P < 0.05; *, P < 0.01 vs. wild type by Tukey's test.