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. 2020 Apr 30;29(2):138–149. doi: 10.5607/en19072

Fig. 4.

Fig. 4

KCC2 antagonist maintains potassium homeostasis in mouse MIR137 cKO neurons. (A) Representative traces of action potentials in response to step current injections in primary neurons at DIV-14. Membrane potential was maintained at approximately –65 mV. Step currents were injected from -50 pA to +300 pA in 50 pA increments (bottom panel). WT, n=21; cKO, n=32; cKO+VU0240551, n=26. (B) Representative traces of whole-cell currents in voltage-clamp mode. Primary neurons were held at -70 mV. Step depolarization from -80 mV to +60 mV at 10-mV intervals was delivered (bottom panel). Insets showing respective traces on an expanded scale. WT, n=23; cKO, n=28; cKO+VU0240551, n=33. (C) The relationship between voltage and K+ current. (D) The peak amplitude of K+ current was reduced to normal in MIR137 cKO neurons that were treated with VU0240551, a specific antagonist for KCC2. (E~G) Statistics of intrinsic membrane properties in MIR137 WT and cKO hippocampal neurons treated with or without VU0240551. RMP, resting membrane potential (E); Rin, membrane input resistance (F); Cm, capacitance (G). *p<0.05, **p<0.01.