Acute effects of leptin require PI3K signaling in hypothalamic proopiomelanocortin neurons in mice
J. Clin. Invest. Jennifer W. Hill, et al. 118:1796 doi:10.1172/JCI32964 [Go to this article.]

Figure 5
Insulin hyperpolarizes POMC neurons via a PI3K-dependent mechanism. (A) Current-clamp record depicting the hyperpolarization of a POMC neuron from rest by 50 nM insulin. The hyperpolarization was reversible within 15 min of wash to control ACSF. Downward deflections are responses to rectangular current steps. (B) Current-clamp recording at resting membrane potential showing insulin-induced hyperpolarization (50 nM) followed by tolbutamide (200 μM) blockade of the insulin effect. (C) Sample trace illustrating the absence of insulin-induced hyperpolarization in POMC neurons from Pik3r1 POMCKO Pik3r2^–/– mice. (D) Insulin-induced responses of identified POMC neurons from WT and Pik3r1 POMCKO Pik3r2^–/– mice. P = 0.02, Pik3r1 POMCKO Pik3r2^–/– versus WT.