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The traces denote differential signal between either the left frontal parietal electrodes (LF-P) or the right frontal parietal electrodes (RF-P). Note that the frequency of the seizure is 3–6 Hz. All subjects were 2 months of age or older at the time of the recordings. (B) Higher resolution tracing illustrating the spike and wave components of the ictal event from the cortex of an LN3-1 transgenic mouse. (C) Comparison of the spontaneous SWD activity between the different transgenic mouse lines. Although the frequency of the seizure was consistent between the different lines, the amount of seizure activity per hour differed significantly between the different lines. Note that the amount of seizure activity present in each line correlates with the amount of immunoreactive transgene expressed within each line (see Figure 1). Data are presented as the mean and standard error of the seizure duration per hour of recording from n=10 (LN2-4); n=11 (LN3-5); n=10 (LN2-3); and n=12 (LN3-1) transgenic mice. (D) The pharmacological responsiveness of the spontaneous SWD in the GABABR1a transgenic mice is consistent with absence epilepsy. The cumulative SWD duration in transgenic line LN3-1 was measured for 1 h either following saline injection or following the administration of the proabsence drug γ-butyrolactone (GBL), the GABABR agonist (−)baclofen (BAC), the GABABR antagonist, CGP 35348 (CGP), or the anti-absence drug ethosuximide (ETO). As shown in the figure, the duration of the SWD was significantly (p<0.01, n=8–10) reduced by pretreatment with either ETO or CGP and exacerbated by GBL or BAC. Note that the injection of the control saline was sufficient to reduce SWDduration (compare panels C and D). Asterisks denote significant differences from their littermate wild type (p<0.05 student’s unpaired t-test). (With Permission from Wu et al. Neurobiology of Disease 26 (2007) 439–451)