Table 2.
Treatment | Spike onset (min) | Amplitude (mV) | Burst onset (min) | Burst frequency (Hz) | Burst duration (sec) |
---|---|---|---|---|---|
KA (i.p.) | 16.17 ± 3.66 | 3.14 ± 0.44 | 36.68 ± 6.73 | 1.27 ± 0.36 | 1.88 ± 0.34 |
Retigabine 5 mg/kg (pre-injection) | 46.04 ± 11.85* | 0.391 ± 0.25 | 22 ± 2.2 | 0.45+0.69* | 0.94 ± 0.26 |
Retigabine 2 mg/kg (post-injection) | - | 0.032 ± 0.024* | 18.7 ± 4.58 | 0.12 ± 0.01** | 0.62 ± 0.54* |
Retigabine 5 mg/kg (post-injection) | - | 3.51 ± 0.32 | 43.26 ± 5.31* | 4.97 ± 1.02** | 1.48 ± 1.67 |
KA (i.c.) | 0.16 ± 0.028 | 4.01 ± 0.55 | 18.18 ± 2.89 | 1.49 ± 0.40 | 0.89 ± 0.14 |
RGB (0.25 μg/L)+KA | 0.18 ± 0.068 | 0.863 ± 1.66 | 28.47 ± 4.08** | 0.03 ± 0.21** | 0.22 ± 85 |
RGB (1 μg/L)+KA | 0.80 ± 0.36 | 3.64 ± 0.48 | 11.9 ± 1.68** | 2.15 ± 0.32* | 1.33 ± 0.12* |
KA was administered by intraperitoneal or intrahippocampal injection to adult Sprague Dawley rats and EEG recordings were performed with in-depth hippocampal electrodes. Lower doses were anticonvulsant, whereas; higher doses were proconvulsant. The onset to spike activity was delayed with i.p. administration; attenuation of spike and wave activity was observed with either route of injection. Due to a wide range of spike amplitudes EEG amplitude was measured within a range to exclude signals below 0.1 mV or above 18 mV. Bars are means ± SEM of 90 min of tracing per animal per group.
p<0.05,
p<0.01. EEG, electroencephalogram; KA, kainic acid; RGB, retigabine