Fig. 6

CLC-3 channel blocker gluconate potently inhibits neonatal seizure activity in vivo. a Representative EEG trace showing recurrent epileptic burst discharges from a P12 rat after KA injection (2 mg/kg, i.p.), which was followed by saline injection (0.1 ml/10 g, i.p.) with 10 min interval. b Expanded view of epileptic burst discharges from the box in a. c, d Representative EEG trace (P12 rat) showing that NaGluc injection (2 g/kg, i.p.) at 10 min after KA injection (2 mg/kg, i.p.) significantly inhibited epileptic burst discharges. e, f Representative EEG trace showing a modest effect of phenobarbital (25 mg/kg, i.p.) on epileptic burst activities in neonatal rat (P12). g, h Representative EEG trace showing the effect of bumetanide (0.2 mg/kg, i.p.) on epileptic burst activities in neonatal rat (P12). i-l In adult mice, KA injection (10 mg/kg, i.p.) also induced robust epileptic burst activities as shown in EEG recordings (i, j), but NaGluc (2 g/kg, i.p.) only showed modest effect on KA-induced epileptic burst activities (k, l). m Summarized data in neonatal animals showing the averaged EEG power (5-min time window) before and after KA injection, followed by injection of saline (black), NaGluc (green), phenobarbital (magenta), or bumetanide (blue). Note that NaGluc significantly inhibited the power of EEG increase induced by KA. Compared to control groups, the EEG power was reduced 72.4% by NaGluc (P < 0.01, unpaired Student’s t-test), 39.6% by phenobarbital (P < 0.04, unpaired Student’s t-test), and 52.8% by bumetanide (P < 0.04, unpaired Student’s t-test) for the last 20 min of drug administration. n In adult animals, the average power in the last 20 min was reduced 36.2% by NaGluc (P < 0.03, unpaired Student’s t-test). In both panels m and n, the black arrowhead indicates the KA injection, and the red arrowhead indicates drug injection. Data are mean ± s.e.m