Electrophysiological characteristics of RIPCre and POMC neurons in response to insulin and leptin. (A) Representative recordings from individual arcuate neurons are shown for POMCCreZEG (A–C, I, and J) and RIPCreZEG (D–H). Leptin (50 nM) and insulin (10 nM) were pressure-ejected (2–5 psi) for 60 seconds (as denoted by arrows). (A) Leptin depolarizes the POMCCreZEG neuron, and this is associated with significant attenuation of spike amplitude. The recording from the neuron shown in B was hyperpolarized to subthreshold potentials by injection of constant current (2–5 pA) through the recording electrode. Application of leptin depolarized and increased the firing rate of the neuron. (C) Diary plot of spike frequency for the neuron shown in B. In contrast, leptin had no effect on membrane potential (D) and spike frequency (E) in RIPCreZEG neurons. Insulin caused depolarization of the RIPCreZEG neuron (F) and increased spike frequency (G), with spike attenuation. As shown in H, the neuron was hyperpolarized to subthreshold potentials as above, and application of insulin clearly depolarizes this neuron with a large increase in spike frequency. In contrast, insulin caused hyperpolarization of POMCCreZEG neurons (I), which was accompanied by a reduction in firing rate (J).