Extended Data Fig. 6: Kir2.1 expression causes neuron inhibition.
From: Profound and redundant functions of arcuate neurons in obesity development
a–g, Brain slices from Vgat-Cre mice (9–10 weeks of age) with prior injections of AAV-DIO-Kir2.1-p2A-dTomato or control vectors to the Arc were used for electrophysiological recording. Recorded neurons from both groups were analyzed for comparison in resting membrane potential (REM, a, n = 21 (control) or 16 (Kir2.1), t = 5.978, df=35, **p < 0.0001, 2-sided unpaired Student’s t test), in percentage of neuron with spontaneous AP firing (b) and in input resistance (c, n = 21 (control) or 16 (Kir2.1), t = 6.892, df=31, **p < 0.0001). d, e, Representative traces showing action potential firing with step wise current injections at the 5pA increment in control (d) and Kir2.1 (e) mice. f, g, Comparison in Rheobase (minimal currents required for AP firing) (f, n = 21 (control) or 16 (Kir2.1), t = 4.660 df=31, **p < 0.0001, 2-sided unpaired Student’s t test) and AP firing threshold (g, n = 21 (control) or 16 (Kir2.1), t = 7.071 df=4, *p = 0.0265, 2-sided unpaired Student’s t test) between the 2 groups. All data presented as mean + /-sem.
