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. 2019 Jul 31;28:120–134. doi: 10.1016/j.molmet.2019.07.008

Figure 1.

Figure 1

Liraglutide depolarizes LepR expressing POMC neurons in arcuate nucleus of hypothalamus. (A) Brightfield illumination of POMC-hrGFP::Lepr-cre::tdtomato neuron from PLT mice. (B) and (C) The same neuron under FITC (hrGFP) and Alexa Fluor 594 (tdtomato) illumination. (D) Complete dialysis of Alexa Fluor 350 from the intracellular pipette. (E) Merge image illustrates colocalization of hr-GFP, tdtomato, and Alexa Fluor 350 indicative of LepR expressing (white arrows) and non LepR expressing (blue arrows) POMC neurons. (F) Electrophysiological study demonstrates a POMC-hrGFP::Lepr-cre::tdtomato (green/red) neuron that is depolarized in response to liraglutide (1 μM). (G) Dosage response of liraglutide on LepR-expressing POMC neurons. (H) Traces showing decreased voltage deflection and increased action potential frequency after liraglutide application. (I) Current versus voltage (I–V) plot illustrating a characteristic decrease in input resistance subsequent to liraglutide application. Shown are responses before (ACSF) and during liraglutide application. (J) Representative trace showing pretreatment with TTX (2 μM) and synaptic blockers (SB) do not abrogate liraglutide-induced depolarization of LepR-expressing POMC neurons. (K) Representative trace showing that GLP 1 depolarizes LepR-expressing POMC neurons. (L) Representative trace showing that pretreatment with TTX (2 μM) and synaptic blockers do not abrogate liraglutide-induced depolarization of LepR-expressing POMC neurons. (M) Histogram summarizing the acute effect of liraglutide on the membrane potential of POMC neurons which express LepR (G&R: LepR expressing POMC neurons). Data are expressed as mean ± SEM.