Fig. 4.

Bumetanide blocked PTZ-induced post-traumatic seizures. a Representative traces from wild type, wild type with TBI, and with/without i.p. injection of bumetanide 30 min before application of PTZ. Inlets in red are extension of the EEG traces. Lower panels are power spectra of seizure activity corresponding to the traces above, red graph is before, and green graph is after PTZ. b A schematic model showing the putative effects of PTZ-induced blockade of GABA receptors lowered the threshold of NKCC1 co-transporters-induced seizures, and bumetanide can reverse the effects of NKCC1-induced seizures. c Normalized power of EEG after i.p. injection of PTZ, averaged data from five mice from each group. The power of EEG was analyzed with power spectrum in Clampfit, and the total power at different frequency was added together to get normalized power. d Histogram comparing the latency of seizures in the groups (**P < 0.01, ANOVA with Newman–Keuls test, N = 5 animals). e, f Histograms comparing the duration and maximal amplitude (averaged top 5 %) of neuronal seizure activity detected within the 60-min observation period after application of PTZ (**P < 0.01, ANOVA with Newman–Keuls test, N = 5 animals)