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Fig. 7 | Molecular Brain

Fig. 7

From: Gluconate suppresses seizure activity in developing brains by inhibiting CLC-3 chloride channels

Fig. 7

CLC-3 Cl channels regulate EGABA during epileptic stimulation in neonatal neurons. a Gramicidin-perforated recordings revealed a depolarizing shift in the GABAA-R reversal potential (EGABA) in CA3 neurons after induction of epileptiform activity in 0 Mg2+ aCSF. b Bath application of NKCC1 inhibitor bumetanide induced a hyperpolarizing shift in EGABA in normal aCSF, but did not abolish the depolarizing shift of EGABA induced by 0 Mg2+ aCSF. c KCC2 inhibitor VU0240551 had no effect on the EGABA under normal aCSF, and showed no effect on the depolarizing shift induced by 0 Mg2+ aCSF. d Gluconate strongly inhibited the depolarizing EGABA shift induced by 0 Mg2+ aCSF. Gluconate itself did not affect the EGABA in normal aCSF. e In CLC-3 KO mice, EGABA did not change when treated with 0 Mg2+ aCSF. The dash line in panels b-e shows the control I-V plot in normal aCSF in A (black line). (F) Quantified data showing the EGABA changes under various conditions in neonatal CA3 pyramidal neurons (P8–9). g Bar graphs showing EGABA changes in adult CA3 pyramidal neurons. Note that NaGluc (20 mM) could not abolish the EGABA shift induced by 0 Mg2+ aCSF in adult animals. Data are shown as mean ± s.e.m. ** P < 0.01, *** P < 0.001

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