Download original image
Fig. 1.

MiR-137 deficiency impairs K+ efflux of potassium in primary mouse hippocampal neurons. (A) Phase-contrast images of primary mouse hippocampal neurons during patch clamp recordings at DIV 14. (B) Representative traces of action potentials in response to step current injections in primary mouse hippocampal neurons at DIV 14. Membrane potential was maintained at approximately -40 mV. Step currents were injected from -50 pA to +250 pA in 50 pA increments (middle panel). All neurons elicited multiple action potentials upon the injection of depolarizing currents. (C) Representative traces of whole-cell currents in voltage-clamp mode. Primary neurons from MIR137 WT or cKO mice were held at -70 mV. Step depolarization from -80 mV to +60 mV at 10-mV intervals was delivered (middle panel). Insets were respective traces on an expanded scale. (D) Characterization of action potentials generation properties in terms of spikes frequency with current-pulse amplitude, recorded from primary mouse hippocampal neurons of MIR137 WT or cKO mice (n=12 and 9, respectively). (E~G) Statistics of intrinsic membrane properties of MIR137 WT and cKO neurons (n =14 and 9, respectively). RMP, resting membrane potential (E); Rin, membrane input resistance (F); Cm, capacitance (G). (H) The relationship between voltage and K+ current (WT, n=12; cKO, n=8). (I) The peak amplitude of K+ current was elevated in MIR137 cKO neurons. *p<0.05.

Exp Neurobiol 2020;29:138~149
© Exp Neurobiol