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. 2015 Sep 18;6:8237. doi: 10.1038/ncomms9237

Figure 7. Model depicting the crosstalk between PKA and leptin signalling in hypothalamic neurons.

Figure 7

During a fast, PKA is activated by nutritional signals acting through an unidentified Gs-coupled GPCR pathway. PKA activation leads to phosphorylation of CREB, which promotes Socs3 transcription when PSTAT3 is present. In the fed state, leptin is increased and stimulates the phosphorylation of STAT3. Leptin may also stimulate the activation of a phosphodiesterase leading to the degradation of cAMP. PSTAT3 and PCREB synergistically induce Socs3 transcription and production of the negative regulator of JAK2 kinase activity. RIIβ−PKA deficiency or expression of the dominant negative PKA allele, RIαB, disrupts basal and fasting-induced CREB phosphorylation inhibiting Socs3 induction and enhancing leptin signalling in the hypothalamus.